0849320518

COMPARTMENT
SYNDROMES
Diagnosis, Treatment,
and Complications
2051_C00.fm Page 2 Tuesday, October 14, 2003 11:28 AM
COMPARTMENT
SYNDROMES
Diagnosis, Treatment,
and Complications
Jorma Styf, M.D., Ph.D.

University of Gteborg
Gteborg, Sweden
CRC PR E S S
Boca Raton London New York Washington, D.C.
Library of Congress Cataloging-in-Publication Data

Styf, Jorma
Compartment syndromes : diagnosis, treatment, and complications / by Jorma Styf.
p. cm.
Includes bibliographical references and index.
ISBN 0-8493-2051-8 (alk. paper)
1. Compartment syndrome. I. Title.
RC951.S89 2003
617.58dc22
2003058469
This book contains information obtained from authentic and highly regarded sources. Reprinted material
is quoted with permission, and sources are indicated. A wide variety of references are listed. Reasonable
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2004 by CRC Press LLC
Illustrations Jorma Styf
No claim to original U.S. Government works
International Standard Book Number 0-8493-2051-8
Library of Congress Card Number 2003058469
Printed in the United States of America 1 2 3 4 5 6 7 8 9 0
Printed on acid-free paper
Preface
This book is for physicians, nurses, and physiotherapists who treat patients with
injuries that are associated with acute compartment syndrome. It is also for physicians and staff personnel who see patients with chronic musculoskeletal pain induced
by exercise. Despite the differences in the clinical appearance and etiology of acute
and chronic syndromes, a common pathophysiological basis ties them together.
Patients with acute compartment syndrome are seen within many medical elds,
e.g., surgery, orthopedics, internal medicine, sports medicine, and psychiatry.
Patients with chronic compartment syndrome are seen by physicians practicing
sports medicine and by general practitioners. I hope that this book will facilitate the
diagnosis and treatment of compartment syndromes. Most of the information in the
book can also be used during basic training for medical students and nurses.
The work to combine the knowledge of others with my own on acute and chronic
compartment syndromes has been stimulating. Compartment Syndromes is based on
1200 scientic publications. I am grateful to the many colleagues who shared their
difcult patient cases of trauma and chronic pain with me. I hope my book will be
helpful for both old and new colleagues. I gladly accept pedagogic and other
comments on the book to improve the future mediation of knowledge on compartment syndromes.
Jorma Styf, M.D., Ph.D.
University of Gteborg, Sweden
Author
Jorma Styf, M.D., Ph.D., is an associate professor of orthopedic surgery at the
University of Gteborg, Sweden. He graduated from the medical school at Gteborg University in 1974. He trained in general surgery and orthopedic surgery at
hospitals in Mlndal, Vrnesborg, Trollhttan, and Gteborg. Dr. Styf defended
his Ph.D. thesis on chronic leg compartment syndrome in 1986 and has been an
associate professor in orthopedic surgery at Sahlgrenska University Hospital,
Gteborg, since 1988. He furthered his professional and scientic training at
University of California, San Diego, in 19881989 and at NASA, Ames Research
Center, California, in 19931994. His present interests include occupational orthopedics, sports medicine, and surgery for knee arthritis. Dr. Styf currently holds a
position as senior consultant at the Department of Orthopedics, Sahlgrenska University Hospital, Gteborg, Sweden.
Acknowledgment
I would like to acknowledge the many colleagues who over the years shared their
questions on patients with difcult musculoskeletal pain or complex trauma cases.
Thanks to Annette Dahlstrm for drawing Figures 4.5, 6.11, and 15.3 and to
Martin Styf for redrawing the original pressure curves and scanning most of the
illustrations in this book.
2051_bookTOC.fm Page 1 Monday, October 6, 2003 2:15 PM
Contents
Chapter 1
Denitions and Terminology ...............................................................1
Intramuscular Pressure.....................................................................................1
Edema...............................................................................................................2
Compartment and Compliance ........................................................................2
Compartment Syndromes.................................................................................3
Acute Compartment Syndrome..............................................................5
Chronic Compartment Syndromes .........................................................5
Other Conditions of Abnormally Elevated Tissue Hydrostatic Pressure........6
Ischemic Contracture .......................................................................................6
Crush Syndrome...............................................................................................6
The Interstitial Space .......................................................................................6
References ........................................................................................................7
Chapter 2
Historical Perspectives of Acute Compartment Syndrome .................9
Introduction ......................................................................................................9
Extrinsic Pressure.............................................................................................9
Inammation and Hyperemia ..........................................................................9
Intrinsic Pressure............................................................................................10
Venous Hypertension .....................................................................................10
Arterial Injury and Spasm..............................................................................11
Exercise ..........................................................................................................11
Intramuscular Pressure Measurements ..........................................................12
Treatment of Acute Compartment Syndrome and Ischemic Contracture.....12
References ......................................................................................................13
Chapter 3
Etiology and Pathogenesis of Acute Compartment Syndrome .........17
Introduction ....................................................................................................17
Increased Volume of the Compartment Contents..........................................17
Fractures ...............................................................................................17
Soft Tissue Trauma...............................................................................18
Surgical Treatment................................................................................19
Exercise.................................................................................................19
Other Reasons for Increased Volume...................................................20
Prolonged Ischemia........................................................................................20
External Compression ..........................................................................20
Arterial Occlusion ................................................................................22
Limb Elevation .....................................................................................22
Decreased Size of the Compartment .............................................................22

Fascial Defect .......................................................................................22
Burn Injury ...........................................................................................23
Other Etiologies .............................................................................................23
Summary ........................................................................................................23
References ......................................................................................................24
Chapter 4
Pathophysiology of Acute Compartment Syndrome .........................33
Introduction ....................................................................................................33
Theories on Local Regulation of Muscle Blood Flow..................................33
Perfusion Pressure ................................................................................33
Microvascular Occlusion......................................................................35
Critical Closing Pressure......................................................................35
Tidal Wave ............................................................................................35
Arterial Spasm ......................................................................................36
Pathophysiology of Abnormally Increased Intramuscular Pressure ............37
Arterial Blood Pressure ........................................................................37
Venous Blood Pressure.........................................................................37
Muscle Blood Flow ..............................................................................37
Muscle Oxygenation.............................................................................37
Neuromuscular Function ......................................................................38
Hypotension and Limb Elevation ..................................................................38
Arterial Blood Pressure ........................................................................39
Venous Return ......................................................................................39
Interstitial Hydrostatic Pressure ...........................................................39
Neuromuscular Function ......................................................................39
Summary ........................................................................................................39
References ......................................................................................................40
Chapter 5
Diagnosis of Acute Compartment Syndrome....................................45
Introduction ....................................................................................................45
Stages of Acute Compartment Syndrome .....................................................45
Symptoms and Signs of Increased Intramuscular Pressure (Stage I)....45
History.........................................................................................45
Physical Examination .................................................................46
Symptoms and Signs of Inadequate Local Tissue
Perfusion (Stage II) ..............................................................................46
History.........................................................................................46
Physical Examination .................................................................47
Symptoms and Signs of Neuromuscular Dysfunction (Stage III) ......48
History.........................................................................................48
Physical Investigation .................................................................48
Location of Acute Compartment Syndromes ................................................48
Leg Compartments ...............................................................................48
Anatomy......................................................................................48
Etiology .......................................................................................49
Clinical Findings in the Anterior Compartment of the Leg ......49
Clinical Findings in the Lateral Compartment of the Leg ........49
Clinical Findings from the Posterior Compartments
of the Leg .................................................................................50
Foot Compartments ..............................................................................50
Anatomy......................................................................................50
Etiology .......................................................................................51
Clinical Findings.........................................................................52
Thigh Compartments ............................................................................52
Anatomy......................................................................................52
Etiology .......................................................................................53
Gluteal Compartments..........................................................................54
Anatomy......................................................................................54
Etiology .......................................................................................54
Lumbar Paraspinal Compartments .......................................................55
Anatomy......................................................................................55
Etiology .......................................................................................55
Shoulder Compartments .......................................................................56
Anatomy......................................................................................56
Etiology .......................................................................................56
Upper Arm Compartments ...................................................................56
Anatomy......................................................................................56
Etiology .......................................................................................57
Forearm Compartments ........................................................................57
Anatomy......................................................................................57
Etiology .......................................................................................57
Hand Compartments.............................................................................58
Anatomy......................................................................................58
Etiology .......................................................................................59
Additional Diagnostic Tools ..........................................................................59
Intramuscular Pressure Measurement ..................................................59
Direct Nerve Stimulation .....................................................................60
Imaging Techniques..............................................................................60
Pulse Oxymetry ....................................................................................60
Stimulation by Vibration ......................................................................60
Differential Diagnosis ....................................................................................61
Summary ........................................................................................................61
References ......................................................................................................62
Chapter 6
Treatment of Acute Compartment Syndromes ..................................67
Introduction ....................................................................................................67
General Principles for Treatment...................................................................67
Step 1 ....................................................................................................67
Step 2 ....................................................................................................68
Step 3 ....................................................................................................68
Step 4 ....................................................................................................68
Step 5 ....................................................................................................69
Step 6 ....................................................................................................69
Indications for Surgical Treatment by Fasciotomy .......................................70
Treatment by Fasciotomy...............................................................................70
Fasciotomy of the Foot ........................................................................71
Fasciotomy of the Leg..........................................................................71
The Parabular Approach ...........................................................71
Double-Incision Fasciotomy.......................................................73
Transinterosseous Decompression..............................................74
Fibulectomy.................................................................................74
Fasciotomy of the Thigh ......................................................................75
Fasciotomy of the Gluteal Compartments ...........................................75
Fasciotomy of the Dorsolumbar Compartment ...................................77
Fasciotomy of Shoulder Muscles.........................................................77
Fasciotomy of the Upper Arm .............................................................77
Fasciotomy of the Forearm ..................................................................78
Fasciotomy of the Volar Compartments .....................................78
Fasciotomy of the Dorsal Compartment ....................................79
Fasciotomy of the Hand .......................................................................79
Postoperative Management ............................................................................80
Edema Reduction..................................................................................80
Secondary Wound Closure by Dermatotraction ..................................80
Secondary Closure by Wire Sutures...........................................80
Silicon or Rubber Bands.............................................................80
External Tissue Extender (ETE).................................................81
Sure-Closure................................................................................82
Other Methods of Dermatotraction ............................................82
Vacuum-Assisted Wound Closure ........................................................83
Skin Grafting ........................................................................................84
Role of Hyperbaric Oxygenation .........................................................84
Summary ........................................................................................................85
References ......................................................................................................85
Chapter 7
Acute Abdominal Compartment Syndrome ......................................91
Introduction ....................................................................................................91
Denition ..............................................................................................91
Incidence...............................................................................................92
Historical Perspectives .........................................................................92
Etiology and Pathogenesis .............................................................................92
Increased Intraabdominal Volume........................................................93
External Compression ..........................................................................93
Decreased Compartment Size ..............................................................93
Pathophysiology .............................................................................................93
Respiratory Function ............................................................................94
Cardiovascular Function.......................................................................95
Cardiac Function.........................................................................95
Arterial Pressure .........................................................................95
Venous Return.............................................................................95
Perfusion Pressure.......................................................................95
Renal Function .....................................................................................96
Visceral Abnormalities .........................................................................96
Neurologic Abnormalities ....................................................................96
Abdominal Wall Abnormalities............................................................97
Measurement of Intraabdominal Pressure .....................................................97
Direct Measurements............................................................................97
Urinary Bladder Pressure .....................................................................97
Intragastric Pressure .............................................................................98
Pressure in the Inferior Vena Cava ......................................................98
Clinical Manifestations ..................................................................................98
Respiratory Symptoms .........................................................................99
Cardiovascular Symptoms....................................................................99
Renal and Visceral Symptoms ...........................................................100
Treatment......................................................................................................100
Nonsurgical Treatment .......................................................................100
Surgical Treatment..............................................................................100
Results .......................................................................................100
Wound Closure..........................................................................101
Chronic Abdominal Compartment Syndrome .............................................101
Summary ......................................................................................................102
References ....................................................................................................102
Chapter 8
Ischemic Contractures......................................................................107
Introduction ..................................................................................................107
Denitions...........................................................................................107
Background.........................................................................................107
Epidemiology......................................................................................108
Etiology and Pathogenesis ...........................................................................108
Pathophysiology ...........................................................................................109
General Principles of Diagnosis, Classication, and Treatment.................110
Symptoms ...........................................................................................110
Clinical Findings ................................................................................110

Muscle Tissue ...........................................................................110
Nerve Tissue..............................................................................110
Classication.......................................................................................110
Mild Contracture.......................................................................111
Moderate Contracture ...............................................................112
Severe Contracture....................................................................112
Treatment ............................................................................................112
Contractures of Leg Muscles.......................................................................112
Contracture of the Anterior Compartment.........................................113
Symptoms..................................................................................113
Clinical Findings.......................................................................113
Treatment ..................................................................................113
Contracture of the Lateral Compartment...........................................114
Symptoms..................................................................................114
Treatment ..................................................................................114
Contracture of the Posterior Compartments ......................................114
Symptoms..................................................................................114
Treatment ..................................................................................115
Contractures of Foot Muscles......................................................................115
Anatomy .............................................................................................116
Symptoms ...........................................................................................116
Treatment ............................................................................................117
Contracture of Thigh Muscles .....................................................................118
Symptoms ...........................................................................................118
Treatment ............................................................................................119
Proximal Release ......................................................................119
Z-Lengthening...........................................................................120
VY Lengthening .....................................................................120
Distal Quadricepsplasty ............................................................121
Results and Complications .................................................................121
Contracture of Gluteal Muscles...................................................................121
Contracture of Hand Muscles ......................................................................121
Anatomy .............................................................................................122
Symptoms ...........................................................................................122
Muscle Tissue ...........................................................................122
Nerve Tissue..............................................................................123
Treatment ............................................................................................123
Interosseous Stripping...............................................................123
Sectioning of Lateral Bands .....................................................123
Release of Extensor Component ..............................................123
Distal Intrinsic Release.............................................................124

Contracture of the Thumb Cleft ..................................................................124
Symptoms ...........................................................................................124
Treatment ............................................................................................124
Contracture of Forearm Muscles .................................................................125
Symptoms ...........................................................................................125
Muscle Tissue ...........................................................................125
Nerve Tissue..............................................................................125
Joints .........................................................................................125
Miscellaneous............................................................................125
Treatment ............................................................................................125
Mild Contractures .....................................................................126
Moderate Contracture ...............................................................126
Severe Contracture....................................................................126
Mixed Contractures...................................................................126
Free Tissue Transfers ...................................................................................126
Summary ......................................................................................................127
References ....................................................................................................127
Chapter 9
The Crush Syndrome .......................................................................131
Introduction ..................................................................................................131
Denitions...........................................................................................131
Historical Review ...............................................................................131
Myoglobin...........................................................................................132
Rhabdomyolysis .................................................................................132
Etiology ........................................................................................................132
Pathogenesis .................................................................................................133
Pathophysiology ...........................................................................................133
Clinical Features ..........................................................................................134
Symptoms and Signs ..........................................................................134
Skin ...........................................................................................134
Muscle .......................................................................................134
Nerve .........................................................................................135
Laboratory Findings ...........................................................................135
Classication.......................................................................................135
Treatment......................................................................................................135
Nonsurgical Treatment .......................................................................135
Surgical Treatment..............................................................................136
Liquefaction and Calcication.....................................................................136
Summary ......................................................................................................137
References ....................................................................................................137
Chapter 10 Etiology and Pathogenesis of Chronic Compartment Syndrome ...141

Introduction ..................................................................................................141
Historical Background........................................................................141
Increased Volume of the Compartment .......................................................142
Exercise...............................................................................................143
Trauma ................................................................................................143
Muscular Hypertrophy........................................................................144
Venous Hypertension..........................................................................144
Myositis ..............................................................................................144
Overload Injuries ................................................................................144
Decreased Compliance of the Compartment...............................................145
External Compression ..................................................................................145
Summary ......................................................................................................146
References ....................................................................................................147
Chapter 11 Pathophysiology of Chronic Compartment Syndrome ...................151
Introduction ..................................................................................................151
Swelling of Muscle Tissue during Exercise ......................................151
Regulation of Local Muscle Blood Flow ....................................................152
Perfusion Pressure (PP)......................................................................152
Microvascular Occlusion....................................................................152
Critical Closing Pressure....................................................................153
Tidal Wave Theory .............................................................................154
Muscle Blood Flow in Chronic Compartment Syndrome ..........................154
Neuromuscular Function in Chronic Compartment Syndrome ..................155
Muscular Oxygenation in Chronic Compartment Syndrome .....................155
Summary ......................................................................................................156
References ....................................................................................................157
Chapter 12 Clinical Diagnosis of Chronic Compartment Syndromes...............161
Introduction ..................................................................................................161
Symptoms and Clinical Findings.................................................................161
Chronic Anterior Compartment Syndrome in the Leg................................162
Symptoms ...........................................................................................162
Signs ...................................................................................................163
Chronic Lateral Compartment Syndrome in the Leg..................................163
Symptoms ...........................................................................................164
Signs ...................................................................................................165
Chronic Posterior Compartment Syndrome in the Leg ..............................165
Symptoms ...........................................................................................166
Signs ...................................................................................................166
Chronic Compartment Syndrome in the Foot..............................................166
Symptoms ...........................................................................................167
Signs ...................................................................................................167
Chronic Compartment Syndrome in the Thigh ...........................................167

Chronic Compartment Syndrome in the Forearm .......................................168
Symptoms ...........................................................................................168
Signs ...................................................................................................168
Chronic Compartment Syndrome in the Hand ............................................169
Symptoms ...........................................................................................169
Signs ...................................................................................................169
Chronic Compartment Syndrome in the Lumbar Spine..............................169
Additional Diagnostic Tools ........................................................................170
Summary ......................................................................................................170
References ....................................................................................................170
Chapter 13 Surgical Techniques and Results of Treatment
of Chronic Compartment Syndromes ..............................................175
Introduction ..................................................................................................175
Pathophysiology of Treatment .....................................................................175
Nonoperative Treatment...............................................................................176
Surgical Treatment .......................................................................................176
Leg Compartments .............................................................................177
Surgical Technique....................................................................177
Endoscopic Fasciotomy ............................................................179
Other Techniques ......................................................................179
Results .......................................................................................180
Complications ...........................................................................180
Foot Compartments ............................................................................181
Results .......................................................................................181
Thigh Compartments ..........................................................................182
Results .......................................................................................182
Forearm Compartments ......................................................................182
Results .......................................................................................184
Hand Compartments...........................................................................184
Lumbar Spine .....................................................................................184
Postoperative Management ..........................................................................184
Summary ......................................................................................................185
References ....................................................................................................185
Chapter 14 Differential Diagnosis of Chronic Leg Pain Induced by Exercise....189
Introduction ..................................................................................................189
Overuse Injuries in the Leg................................................................190
Anterior Leg Pain ...............................................................................190
Posterior Leg Pain ..............................................................................191
Skeletal Muscle Pain ..........................................................................191

Mechanical Pain........................................................................192
Inammatory Pain.....................................................................192
Ischemic Pain ............................................................................192
Miscellaneous............................................................................192
Anterolateral Leg Pain .................................................................................192
Anterior Periostitis (Periostalgia).......................................................192
Etiology .....................................................................................193
Symptoms and Signs ................................................................193
Treatment ..................................................................................193
Entrapment of the Common Peroneal Nerve.....................................194
Treatment ..................................................................................194
Peroneal Tunnel Syndrome ................................................................194
Etiology .....................................................................................195
Treatment ..................................................................................196
Fascial Defects....................................................................................196
Etiology .....................................................................................196
Treatment ..................................................................................196
Stress Fracture of the Anterior Margin of the Tibia..........................197
Etiology .....................................................................................198
Treatment ..................................................................................198
Stress Fractures of the Fibula.............................................................198
Treatment ..................................................................................199
Tendinosis of Extensor Tendons ........................................................199
Instability of the Proximal Syndesmosis ...........................................199
Posterior Leg Pain........................................................................................199
Medial Tibial Syndrome.....................................................................200
Etiology .....................................................................................200
Symptoms..................................................................................201
Clinical Examination ................................................................201
Treatment ..................................................................................202
Muscle Strain Injury (Tennis Leg).....................................................203
Etiology .....................................................................................203
Treatment ..................................................................................204
Accessory Soleus Muscle...................................................................204
Treatment ..................................................................................205
Muscular Hypertension Syndrome.....................................................205
Treatment ..................................................................................206
Stress Fractures of the Posteromedial Margin of the Tibia...............206

Etiology .....................................................................................206
Pathogenesis..............................................................................206
Treatment ..................................................................................207
Entrapment of Popliteal Artery ..........................................................207
Etiology .....................................................................................207
Classication .............................................................................208
Treatment ..................................................................................208
Entrapment of the Tibialis Nerve.......................................................209
Etiology .....................................................................................209
Treatment ..................................................................................210
Entrapment of the Saphenous Nerve .................................................210
Etiology .....................................................................................210
Treatment ..................................................................................210
Entrapment of the Common Suralis Nerves ......................................211
Etiology .....................................................................................211
Treatment ..................................................................................212
Venous Diseases of the Leg.........................................................................212
Venous Insufciency...........................................................................212
Treatment ..................................................................................213
Varicose Veins.....................................................................................213
Venous Claudication...........................................................................213
Thrombophlebitis................................................................................213
Effort-Induced Venous Thrombosis....................................................213
Miscellaneous...............................................................................................214
Combined Symptoms .........................................................................214
Summary ......................................................................................................214
References ....................................................................................................215
Chapter 15 Composition and Function of the Interstitial Space........................221
Introduction ..................................................................................................221
Muscle and Tendon ............................................................................221
Composition of the Interstitial Space ..........................................................221
Function of the Interstitial Space ................................................................223
Extravascular Flow System ................................................................223
Fluid Reservoir ...................................................................................224
Storage Functions ...............................................................................224
Immunological Support ......................................................................224
Elastic Support....................................................................................224
Regeneration of Muscle Tissue ..........................................................224

Force Transmission.............................................................................225
Neuromuscular Transmission .............................................................225
Biomechanics of the Interstitial Space ........................................................225
Forces and Stresses.............................................................................227
Hydrostatic Pressure Generation........................................................227
Intramuscular Pressure as a Measure of Force Generation...............227
Pressures in the Interstitial Space ......................................................228
Interstitial Fluid Pressures..................................................................228
Solid Tissue Pressure..........................................................................229
Total Tissue Pressure ..........................................................................229
Compliance of the Interstitial Space ...........................................................230
Hydraulic Permeability of the Interstitial Space..........................................232
Summary ......................................................................................................232
References ....................................................................................................233
Chapter 16 Measurement of Intramuscular Pressures at Rest ...........................235
Introduction ..................................................................................................235
Measurement Quality...................................................................................235
Accuracy .............................................................................................235
Sensitivity ...........................................................................................236
Linearity, Uniqueness, and Hysteresis ...............................................237
Compliance of the Pressure-Recording System ..........................................237
Catheter Insertion Technique .......................................................................238
Response and Location of the Catheter Tip ......................................239
Tissue Trauma due to Catheter Insertion...........................................239
Catheter Occlusion .............................................................................241
Contact Area of the Catheter..............................................................242
Volume Load ......................................................................................242
Physiologic Reactance........................................................................242
Classication of Catheters for Intramuscular Pressure Measurement ........243
Design of the Catheter Tip.................................................................243
Needle Designs .........................................................................243
Wick Catheter ...........................................................................244
Slit Catheter ..............................................................................244
Myopress Catheter ....................................................................244
Intracath Catheter......................................................................245
Wick-in-Needle .........................................................................245
Location of the Transducer ................................................................245
Fiberoptic Transducer-Tipped Catheter ....................................245
Solid-State Intracompartmental Catheter (STIC).....................245
Codman Catheter ......................................................................246
The Kodiag Catheter.................................................................246
Medium of Signal Transmission ........................................................247
Techniques for Intramuscular Pressure Measurements ...............................247
Injection Techniques...........................................................................248
Infusion Techniques............................................................................249
Noninfusion Techniques .....................................................................250
Intramuscular Pressure Measurements in a Subatmospheric Environment ... 251
Methods for Noninvasive Measurements of Intramuscular Pressure..........251
Summary ......................................................................................................252
References ....................................................................................................252
Chapter 17 Measurements of Intramuscular Pressure during Exercise .............257
Introduction ..................................................................................................257
Dynamic Properties of Pressure-Recording Systems..................................257
Rise Time............................................................................................259
Compliance of Pressure-Recording Systems .....................................261
Natural Frequency ..............................................................................261
Dynamic Testing of Pressure-Recording Systems ......................................262
Transient Step Response ....................................................................262
Sinusoidal Pressure Generator ...........................................................262
Practical Recommendations.........................................................................263
Pressure-Recording Systems ..............................................................263
Catheter Insertion Technique..............................................................263
Check of Catheter Position ................................................................265
Position of the Limb...........................................................................265
Typical Distortions of Intramuscular Pressure Recordings.........................265
Techniques for Intramuscular Pressure Measurements ...............................267
Infusion Techniques............................................................................267
Noninfusion Techniques .....................................................................269
Transducer-Tipped Catheters..............................................................269
Fiberoptic Catheters ..................................................................270
STIC Catheter ...........................................................................271
Codman and Kodiag Catheters.................................................271
Reference Values for Intramuscular Pressures ............................................272
Intramuscular Pressure at Rest before Exercise ................................272
Normal Values...........................................................................272
Abnormal Values.......................................................................272
Muscle Contraction Pressure during Exercise ...................................272
Muscle Relaxation Pressure during Exercise.....................................273
Normal Values...........................................................................273
Abnormal Values.......................................................................273
Mean Muscle Pressure during Exercise.............................................274
Intramuscular Pressure at Rest after Exercise ...................................275
Normal Values...........................................................................275
Abnormal Values.......................................................................275
Intramuscular Pressure Oscillations at Rest after Exercise ...............276
Estimation of Force Generation and Muscle Length
by Intramuscular Pressures ..........................................................................277
Force Generation Estimated by Intramuscular Pressure and EMG.....277

Force Generation and Muscle Length................................................278
Summary ......................................................................................................278
References ....................................................................................................279
Chapter 18 Limb Edema.....................................................................................283
Introduction ..................................................................................................283
Edema Formation .........................................................................................283
Vasogenic Edema................................................................................283
Capillary Hypertension .............................................................284
Low Intravascular Oncotic Pressure.........................................284
Alterations of Microvascular Barriers ......................................284
Myxedema ..........................................................................................285
Lymphedema.......................................................................................285
Edema-Preventing Mechanisms...................................................................285
Edema-Reducing Methods...........................................................................286
Muscle Contractions...........................................................................286
Passive Stretch of Muscle ..................................................................286
External Compression ........................................................................287
Continuous Compression..........................................................287
Intermittent Compression .........................................................287
Limb Elevation ...................................................................................288
Leg and Foot Muscle Pumps .............................................................289
Transplantation of Venous Valves ......................................................290
Hyperbaric Oxygenation ....................................................................291
Summary ......................................................................................................291
References ....................................................................................................291
Index ......................................................................................................................295
2051_C01.fm Page 1 Thursday, October 2, 2003 9:26 AM
Definitions and
Terminology
INTRAMUSCULAR PRESSURE
Intramuscular pressure is defined as the fluid hydrostatic pressure in the interstitial

space of skeletal muscle tissue. In a normally hydrated muscle at rest, this pressure
ranges between 2 and 8 mmHg. Subcutaneously it is normally below atmospheric
pressure. Intramuscular pressure depends on the positions of the subject and the
catheter depth in the muscle.13 Edema, external compression, passive stretch of a
muscle and muscle contraction, or any combination of the four factors increases
intramuscular pressure. Intramuscular pressure can be defined by the Starling equation (Equation 1.1),4 which describes the magnitude and direction of fluid shift (Jc)
over the capillary wall by the two hydrostatic and two osmotic pressures (Figure 1.1):
Jc = Kf [(Pc Pt) b(pc pt)]
(1.1)
where Jc is the net fluid flow across the capillary wall, Kf the capillary filtration
coefficient, Pc the capillary blood hydrostatic pressure, Pt the hydrostatic pressure
in the interstitial fluid, b the capillary membrane reflection coefficient, pc the
capillary blood colloid-osmotic pressure, and pt the osmotic pressure in the interstitial fluid.
At steady state, the capillary net fluid flow is zero. In this situation, hydrostatic
pressure in the interstitial space (Pt) can be expressed as:
Pt = Pc (pc pt)]
(1.2)
Pressure (P) may also be a vector expressed as force (F) per unit area (A). In this
case, pressure has a magnitude and a direction:
P = F/A
(1.3)
Contact pressure (P) acts on a surface (A), e.g., pressure between the bone and an
implant. Contact pressure and frictional forces require physical contact, a surface,
to be transmitted. Forces (F) may also be transmitted through solid components of
the tissues. Body forces such as gravity and electrostatic forces act without physical
contact. Stress (Pascal) is the force (F) per unit area (m2). It is a vector, because it
has a magnitude and a direction. Solid tissues may become strained and deformed
by forces. These forces are sometimes labeled solid pressure.5 In this book, pres-
Compartment Syndromes: Diagnosis, Treatment, and Complications
Capillary
Intravascular
Pa
Pv
Lymph vessel
Interstitial
Fluid flow
Prelymphatic space
Intracellular
Cell
FIGURE 1.1 Schematic illustration of how the two hydrostatic (Pc and Pt) and two osmotic
(c and t) pressures act over the capillary wall. The area within the dotted line indicates
the prelymphatic space. The drawing illustrates the central position of the interstitial fluid
hydrostatic pressure (Pt) and its importance to direct fluid flow among the intravascular,
intracellular, and interstitial spaces.
sure is regarded to be a scalar-like fluid hydrostatic pressure. It has a magnitude

but no direction.
Generally, pressure is defined as the force exerted per unit area. In clinical
practice as well as in physiological experiments, pressure is expressed as millimeter
of mercury (mmHg) or in kiloPascal (kPa). One kPa is ca. 7 mmHg. If it is assumed
that the density of mercury is 13.6 g/cm3, the density of blood is 1.06 g/cm3, and
that of physiological saline 1.04 g/cm3, then 1 mmHg is equal to 12.9 mm blood or
13.1 mm saline, which compare at 0.14 kPa. The hydrostatic pressure of 1 mmHg
at 0C is 1330 dyn/cm2 if the gravitational force is 0.981 m/sec2.
In clinical practice, pressure is measured relative to atmospheric pressure. Some
pressure transducers are sealed. Therefore, they must be recalibrated repeatedly
against atmospheric pressure to avoid errors.
EDEMA
Edema is a sign of overhydration of the interstitial space and is caused by a disturbed
microcirculation or dysfunctional lymph flow, or both.6 Figure 1.2 illustrates the
relation between the degree of interstitial hydration and interstitial fluid hydrostatic
pressure. Abnormally increased intramuscular pressure for any reason during an
extended period of time may jeopardize local tissue nutrition and viability. Patients
might even experience ischemic pain from posttraumatic edema. As opposed to
edema is the condition of dehydration. During dehydration, subcutaneous pressure
decreases rapidly below atmospheric pressure and becomes negative.
COMPARTMENT AND COMPLIANCE

A compartment is a well-defined anatomical space, e.g., the anterior tibial compartment of the leg7 or paravertebral muscles of the dorsolumbar compartment of the
Definitions and Terminology
Interstitial
hydrostatic
pressure
D.
Positive
B.
C.
Atmospheric
100
A.
200
300
Volume %
Negative
FIGURE 1.2 Relation between hydrostatic tissue pressure and volume in the interstitial space.
The curve has three different slopes depending on the degree of tissue hydration. The compliances of the dehydrated (A) and normally hydrated (B) tissues are very low. On the contrary,
at C the compliance is very high in the overhydrated tissue. Finally, when tissue hydration
is excessive (D), compliance decreases again.
back.8,9 Most often, the compartment tissues are contained in relatively unyielding
osteofascial spaces (Figure 1.3).
Compliance of muscle tissue within a compartment describes the relation
between volume and pressure in that space (Figure 1.4). Compliance (C) is defined
as the relative change between pressure (P) and volume (V):
C = (P1 P2)/(V1 V2)
(1.4)
The contents of a compartment are sometimes surrounded by relatively unyielding

osteofascial structures. Intramuscular pressure might increase rapidly when the volume of the contents in an osteofascial space increases (Figure 1.4). In thin, flat
muscles, e.g., the trapezius muscle with a soft epimysium, the compliance value is
high. The compliance of the subcutaneous tissue is even higher.
COMPARTMENT SYNDROMES
Compartment syndrome is a condition in which elevated intramuscular pressure
reduces local blood flow and impairs function of the tissues within that compartment
(Figure 1.5).10,11 The local tissue ischemia produces pain and tissue dysfunction that
persists until the pressure within the compartment is normalized. Symptoms reverse
once the local blood flow corresponds to the demands for nutrition and viability of
the tissues. Two forms of compartment syndrome exist: acute compartment syndrome and chronic compartment syndrome.
Anterior
Tibia
Lateral
Deep posterior
Superficial posterior
FIGURE 1.3 Cross section through the leg illustrating the anterior, lateral, deep posterior,
and superficial posterior compartments with their relatively unyielding osteofascial boundaries. Nerves and vessels running through the compartments are exposed to the same magnitude of hydrostatic pressure as are muscles.
Interstitial
hydrostatic
pressure
Muscle compartment
Subcutaneous tissue
100
200
300
Volume %
FIGURE 1.4 Schematic illustration of compliance in a muscle compartment and in subcutaneous tissue. Compartment muscles are usually more susceptible to volume increase than
subcutaneous tissue.
Pressure
MAP
MAP
Perfusion pressure
Perfusion pressure
PV
Elevated IMP
PV
Normal IMP
Normal hydration
Normal IMP
Edema
FIGURE 1.5 Schematic illustration of perfusion pressure at the capillary level in a normally
hydrated tissue (left) and in an edematous tissue (right). Perfusion pressure is the difference
between mean arterial pressure (MAP) and venous pressure (Pv). Venous pressure within a
compartment cannot be lower than the local intramuscular pressure (IMP). Therefore,
increased intramuscular pressure decreases perfusion pressure within the compartment.
ACUTE COMPARTMENT SYNDROME

Acute compartment syndrome is a severe irreversible form of abnormally elevated intramuscular pressure that leads to tissue necrosis and permanent loss of
function if left untreated. The condition may even be life threatening if several
compartments, i.e., large muscle masses, are affected simultaneously. Common
reasons for acute compartment syndrome include trauma with bleeding into the
compartment, postischemic swelling following arterial injury, and long-term
external compression of the tissues. Treatment includes decompression of the
compartment tissues. Synonyms for acute leg compartment syndrome in previous
literature are anterior tibial pain,12 calf hypertension,13 rhabdomyolysis,14 and
march gangrene.15
CHRONIC COMPARTMENT SYNDROMES

Chronic compartment syndromes are defined as painful conditions in which
increased intramuscular pressure during exercise impedes local muscle blood flow
and impairs the neuromuscular function of the tissues within a compartment.16,17 The
chronic syndrome is a mild reversible form of abnormally increased intramuscular
pressure during exercise. If the patient stops exercising, the symptoms will reverse.
However, if the exercise continues beyond the pain limit and the muscle continues
to swell, an acute irreversible condition might develop.18 Chronic compartment
syndrome is most often diagnosed in athletes, who have a high level of physical
activity.17 Synonyms for chronic compartment syndrome found in literature are
anterior tibial pain,19 chronic anterior tibial compartment syndrome,20 anterior compartment syndrome,21 exertional compartment syndrome,22 recurrent compartmental
syndrome,23 and idiopathic compartment syndrome.24 In this book, the condition is
labeled chronic compartment syndrome.
OTHER CONDITIONS OF ABNORMALLY ELEVATED

TISSUE HYDROSTATIC PRESSURE
Conditions similar to acute compartment syndrome may also develop within other
nonyielding spaces such as the orbital globe (glaucoma), intracranial cavity, intrathoracic cavity (tension pneumothorax), and in the kidney.25 Such conditions have been
described in intraabdominal organs following elevated intraperitoneal pressure.26
High intraperitoneal pressure impairs blood supply of abdominal organs by reducing
local perfusion pressure. Acute abdominal compartment syndrome is defined as
increased intraperitoneal hydrostatic pressure to levels that impair blood perfusion
pressure of intraperitoneal and retroperitoneal organs, and induce respiratory and
cardiovascular dysfunction.
ISCHEMIC CONTRACTURE
Ischemic contracture is a limb deformity that represents one of the final stages of
muscle and nerve fibrosis. It is a local ischemic damage of selective tissues due to
an untreated acute compartment syndrome. In 1981 Von Volkmann first described
the clinical entity in the forearm.27 He proposed that the syndrome was caused by
tight dressings in traumatized limbs. Ischemic contracture may also follow local
arterial injury. Treatment is individualized and may include complex soft tissue
releases of muscles, tendons, and nerves. In late stages, it may require surgery on
bones and joints. In 1980, compartment syndromes in the Index Medicus replaced
the index word anterior compartment syndrome, which was used since 1972. To
date, Volkmanns contracture has been used as an index entry.
CRUSH SYNDROME
Crush syndrome is the system manifestations of an untreated acute compartment
syndrome or by other trauma to the muscle tissue. System manifestations include
renal dysfunction, hypovolemic shock, and cardiac arrhythmia. Crush syndrome is
different from crush injury, which describes a variety of localized traumas to soft
tissues and bones, and which may also threaten tissue nutrition and viability. Patients
with crush injury may have peripheral ischemia, causing crush syndrome without
having acute compartment syndrome.
THE INTERSTITIAL SPACE

The volume of the interstitial space is 15% of the total body volume and is three
times higher than the intravascular space. The interstitial space is the tissue located
between the cells and the vessels. The volume of the space varies between tissues.
The space contains 95% of the volume of cartilage tissue and 5% of muscle tissue.
In muscle tissue, the interstitial network between muscle fibers participates in the
transmission of tensile force to the muscle tendon.
The interstitial space consists of a fluid phase, which includes microscopic
channels that end in the prelymphatic space, and a phase of solid network. The
exchange of fluid between the capillary bed and the cells is transported through the
interstitial space (Figure 1.1). Diffusion is transportation of small molecules along
the concentration gradient. Convection is transportation of solutes along the hydrostatic pressure gradient.
REFERENCES
1. Gershuni, D.H., Yaru, N.C., Hargens, A.R., Lieber, R.L., O'Hara, R.C., and Akeson,
W.H., Ankle and knee position as a factor modifying intracompartmental pressure in
the human leg, J. Bone Jt. Surg., 66-A, 1415, 1984.
2. Nakhostine, M., Styf, J.R., Leuven, S.V., Hargens, A., and Gershuni, D.H., Intramuscular pressure varies with depth: the tibialis anterior muscle studied in 12 volunteers,
Acta Orthop. Scand., 64, 377, 1993.
3. Sejersted, O.M., Hargens, A.R., Kardel, K.R., Blom, P., Jensen, ., and Hermansen,
L., Intramuscular fluid pressure during isometric contraction of human skeletal muscle, J. Appl. Physiol., 56, 287, 1984.
4. Starling, E.H., On the absorption of fluids from the connective tissue spaces, J.
Physiol. (Lond.), 19, 313, 1896.
5. Guyton, A.C., Granger, H.J., and Taylor, A.E., Interstitial fluid pressure, Physiol. Rev.,
51, 527, 1971.
6. Hargens, A.R., Akeson, W.H., Mubarak, S.J., Owen, C.A., Gershuni, D.H., Garfin,
S.R. et al., Tissue fluid pressures: from basic research tools to clinical applications,
J. Orthop. Res., 7, 902, 1989.
7. Edwards, E.A., The anatomic basis for ischemia localized to certain muscles of the
lower limb, Surg. Gyn. Obstr., 97, 87, 1953.
8. Carr, D., Frymoyer, J.W., and Gilbertson, L., The lumbodorsal fascial compartment,
Orthop. Trans., 252, 1984.
9. Styf, J., Pressure in the erector spinae muscle during exercise, Spine, 12, 675, 1987.
10. Matsen, F.A., Compartmental syndrome: a unified concept, Clin. Orthop., 113, 8,
1975.
11. Mubarak, S. and Owen, C.A., Compartment syndrome and its relation to the Crush
syndrome: a spectrum of disease, Clin. Orthop., 113, 81, 1975.
12. Carter, A.B., Richards, R.L., and Zachary, R.B., The anterior tibial syndrome, The
Lancet, 19, 928, 1949.
13. Gaspard, D.J., Cohen, J.L.L., and Gaspar, M.R., Decompression dermotomy: a limb
salvage adjunct, JAMA, 220, 831, 1972.
14. Klock, J.C. and Sexton, M.J., Rhabdomyolysis and acute myoglobinuric renal failure
following heroin use, West J. Med., 119, 5, 1973.
15. Blandy, J.P. and Fuller, R., Ischemic myositis of the leg muscles from exercise., J.
Bone Jt. Surg., 39-B, 679, 1957.
16. Styf, J., Suurkula, M., and Krner, L., Intramuscular pressure and muscle blood flow
during exercise in chronic compartment syndrome, J. Bone Jt. Surg., 69-B, 301, 1987.

17. Styf, J., Chronic exercise-induced pain in the anterior aspect of the lower leg: an
overview of diagnosis, Am. J. Sp. Med., 7, 331, 1989.
18. Bradley, E.L., The anterior tibial compartment syndrome, Surg. Gyn. Obstet., 136,
289, 1973.
19. French, E.B. and Price, W.H., Anterior tibial pain, Br. Med. J., 6, 1290, 1962.
20. Leach, R.E., Hammond, G., and Stryker, W.S., Anterior tibial compartment syndrome:
acute and chronic, J. Bone Jt. Surg., 49-A, 451, 1967.
21. Reneman, R.S., The anterior and the lateral compartmental syndrome of the leg due
to intensive use of muscles, Clin. Orthop. Rel. Res., 113, 69, 1975.
22. Mubarak, S.J., Exertional Compartment Syndrome, Mubarak, S. and Hargens, A.,
Eds., W.B. Saunders, Philadelphia, 1981, p. 209, chap. 14.
23. Veith, R.G., Recurrent compartmental syndromes due to intensive use of muscles, in
Compartmental Syndromes, Matsen, F.A., III, Ed., Grune & Stratton, New York, 1980,
p. 133.
24. Rorabeck, C.H., Macnab, I., and Wadell, J.P., Anterior tibial compartment syndrome:
a clinical and experimental review, Can. J. Surg., 15, 249, 1972.
25. Stone, H.H. and Fulenwider, J.T., Renal decapsulation in the prevention of postischemic oliguria, Ann. Surg., 186, 343, 1977.
26. Schein, M., Wittman, D.H., Aprahamian, C.C., and Condon, R.E., The abdominal
compartment syndrome: the physiological and clinical consequences of elevated intraabdominal pressure, J. Am. Coll. Surg., 180, 745, 1995.
27. Volkmann, R., Ischaemic muscle paralyses and contractures, Clin. Orthop., 50, 5,
1881.
2051_C02.fm Page 9 Monday, October 6, 2003 1:59 PM
Historical Perspectives
of Acute Compartment
Syndrome
INTRODUCTION
In 1667 Stenson rst described ischemic paralysis in the lower limb.1 He observed
paralysis of the posterior extremities of an animal following occlusion of the abdominal aorta. A patient with ischemic contracture, presumably from a compartment
syndrome, was reported in 1850 by Hamilton according to Hildebrand.2 Research
on the pathologic process of ischemic contractures of the extremities started more
than 150 years ago. Theories on external compression, inammation, arterial injury
and spasm, venous obstruction, and tissue pressure have been investigated thoroughly
for the past 100 years. The effects of strenuous exercise as a cause of acute compartment syndrome were described in the 1940s.3,4
Historical perspectives of the evolution of different theories on etiology, pathogenesis, pathophysiology, and treatment of acute compartment syndrome are discussed
in this chapter (Figure 2.1). Reviews of the historical perspectives on the exciting
search for clarity regarding ischemic contractures have been presented previously.5,6
EXTRINSIC PRESSURE
In a classic paper from 1881, Von Volkmann presented the hypothesis that brosis and
contracture of the muscle in an injured extremity were caused by interrupted arterial
blood supply.7 He observed cases where the contracture followed arterial ligature, contusion to extremities, and prolonged external compression (or extrinsic pressure). Since
then, prolonged external compression has been accepted as a cause of muscle ischemia.
In 1884, Leser reported seven patients in whom muscle contracture followed
the application of constricting bandages.8 He investigated the effects of ischemia on
muscles in animal experiments and concluded that contractures and paralysis were
caused by decreased oxygen tension in muscle tissue. It is fair to say that Volkmann
described the clinical presentation and Leser introduced a laboratory model of
ischemic contracture of limb muscles. More recently, external compression has been
used as a model of compartment syndrome in humans.9,10
INFLAMMATION AND HYPEREMIA

Based on Lesers reports, in 1888 Petersen suggested that an inammatory process
caused muscle contracture.11 In 1900, Bernays showed that lymphocytes and
9
10
Extrinsic
pressure
Intrinsic
pressure
Venous
hypertension
Experimental models of
compartment syndromes
Positive tissue pressure
Subatmospheric tissue pressure

Exercise-induced acute
compartment syndrome
Inflammation and hyperemia
Chronic compartment syndrome
Decreased muscle blood flow

and tissue oxygenation
Arterial injury
and spasm
Secondary wound closure
Decompression by fasciotomy
1880
1900
1920
1940
year
1960
1980
2000
FIGURE 2.1 Summary of time aspects on the beginning of different views and theories on
pathophysiology, pathogenesis, and treatment of acute and chronic compartment syndromes.
Extrinsic pressure is currently regarded as increased tissue pressure due to prolonged
external compression.
monocytes surrounded the ischemic contracture of the muscle.12 In 1901, Wallis

demonstrated that neurologic damage and muscle scarring was induced by hyperemia.13 He suggested that hyperemia was the critical feature in creating Volkmanns
ischemic contracture.
INTRINSIC PRESSURE
Increase of intrinsic pressure following hemorrhage and effusion into the muscle
was suggested by Littlewood14 in 1900 and by Murphy15 in 1906. Murphy thought
that venous obstruction rather than arterial injury caused the muscular contracture.
Later in the 1970s, Rorabeck and McNab as well as Scheridan and Matsen created
elevated intracompartmental pressure by infusing a hypertonic mannitol solution
into the anterior compartment of dogs.16,17 The clearance of Tc 99 from the anterior
tibial muscle decreased with increasing intramuscular pressure.
VENOUS HYPERTENSION
Hildebrand in 1906 and Murphy in 1914 suggested that effusion by elevated venous
pressure increased pressure in the muscle.2 Brooks produced ischemic contracture by
obstructing venous return in a laboratory model.18 He experimentally created muscle
Historical Perspectives of Acute Compartment Syndrome
11
necrosis by venous ligature. Arterial ligature did not create any necrosis. Jepsons
results in the 1920s indicated that contracture deformity was due to a combination of
factors, of which impaired venous ow was the most important.19 Furthermore, he
demonstrated that decompression of the limb within a few hours of the start of vein
obstruction prevented contracture formation. Recently, venous hypertension by vein
obstruction has been used to study the effects of abnormally increased intramuscular
pressure on neuromuscular function and muscle blood ow in human legs.2022
ARTERIAL INJURY AND SPASM

Bardenheuer described the relation between ischemic state and arterial wall injury
in 1906.23 Leriche suggested that the mechanism of arterial spasm, caused by a
nervous reex mediated through the sympathetic nervous system, was the pathogenetical mechanism of ischemic contracture.24 Theories regarding venous obstruction
were challenged also by Grifths in 1940, who stated that Volkmanns ischemic
contracture was due to arterial injury with reex spasm of the collateral circulations.25 This concept was supported by Sirbu et al. in 1944, who presented a case
of bilateral gangrene in the anterior compartment of the leg, which was developing
merely from marching. They explained the gangrene by vulnerability of the anterior
tibial artery in the anterior compartment.26 Although Kinmonth et al. in 1949 showed
that it was not possible to precipitate arterial spasm experimentally,27 the concept
of arterial spasm was popular for many years and was later supported by Seddon28
and by Gardner.29 The theory of postischemic swelling in a limb following restoration
of arterial ow had already been suggested by Rowlands30 in 1910. Currently, the
condition is regarded as a reperfusion syndrome.
EXERCISE
Severin in 1943 and Vogt in 1943 rst described the anterior tibial syndrome.3,4 The
anterior tibial syndrome was dened as the triad of (1) necrosis of the anterior tibial
muscle, (2) paralysis of the extensor digitorum brevis muscle, and (3) anesthesia of
the rst interdigital cleft of the foot.31,32 Today, anterior tibial syndrome should rather
be termed as an untreated acute compartment syndrome of the leg. The term march
gangrene is used synonymously with anterior tibial syndrome.26 In a review of the
literature, Bradley reported in 1973 that 33% of all anterior tibial syndromes were
induced by exercise.6 Sixteen percent of these patients had a long history of recurrent
pain induced by exercise in the anterior compartment predating the episode. These
patients had participated in physical activities such as football, long marches, and
other strenuous exercises. The ndings suggested that a less harmful recurrent form
could induce the anterior tibial syndrome.
Carter and co-workers rst described a reversible form of anterior tibial syndrome in 1949.31 Mavor rst described the chronic, recurrent, reversible form of
anterior tibial syndrome in 1956.33 The existence of this syndrome was questioned
by Grifths in 1956 and by Grunwald and Silberman in 1959.34,35 However, French
and Price in 1962 and Reneman in 1968 conrmed the existence of the syndrome
by measuring intramuscular pressure and local muscle blood ow.36,37
12
INTRAMUSCULAR PRESSURE MEASUREMENTS

Landerer performed the rst measurement of interstitial tissue uid hydrostatic
pressure in 1884 with a needle manometer technique.38 Some years later, Starling
(1896) measured the tissue uid pressure by injecting several milliliters of uid
through a needle into subcutaneous tissue.39 He observed how the pressure fell to a
plateau of 5 mmHg. Later the needle injection technique was improved by Henderson
et al., who injected one or two cubic millimeters during measurements to make sure
the needle was not occluded.40 Burch and Sodeman improved the technique by
introducing side holes in the needle.41 They injected only 0.1 to 0.5 mm3 at pressure
recordings. In 1938, Wells and co-workers showed that intramuscular pressure
increased to about 40 mmHg during venous stasis induced by a tourniquet inated
to about 70 mmHg. They also showed that intramuscular pressure during a muscle
contraction reached 90 mmHg. The needle injection technique was later popularized
for clinical use.37,42,43 However, this method of pressure recording has been questioned.4446
In 1941, McMaster found that uid moved into the cutaneous tissue at atmospheric pressure.47 He measured pressure by a 0.3-mm (30-gauge) hypodermic
needle that was connected to a 0.2-mL micropipette. The uid meniscus in the pipette
moved intermittently toward the tissue. This was probably the rst report indicating
that interstitial uid pressure is subathmospheric. However, the concept of slightly
positive interstitial uid hydrostatic pressures in the range of 1 to 5 mmHg in the
human body prevailed until the 1960s.
In 1963, Guyton introduced the concept of a negative interstitial uid pressure
recorded by the chronically implanted capsule.48 Negative tissue pressures were also
recorded by Scholander et al. in 1968 by a wick catheter method.49 These results
were also conrmed by Snashall et al. and Wiederhielm,50,51 but they suggested that
the negative hydrostatic pressure was largely due to osmotic pressure of the interstitium. Currently, it is generally agreed that certain tissues, e.g., subcutaneous tissue,
have negative tissue uid pressures whereas others have positive pressures. Muscle
tissue pressure is considered to be positive by most authors,45,52,53 but a slightly
negative pressure of about 1 mmHg has been reported.54
TREATMENT OF ACUTE COMPARTMENT SYNDROME

AND ISCHEMIC CONTRACTURE
Surgical decompression by fasciotomy as a treatment for acute compartment syndrome was rst suggested by Bardenheuer in 1906.23 The treatment was based on
his theory that the ischemic state was due to a combination of arterial injury, venous
stasis, and edema. In 1914, Murphy suggested treatment by fasciotomy to prevent
the contracture state from developing.15 Later, in the 1920s, Jepson performed
fasciotomy in dog experiments.19 He demonstrated that decompression of the limb
within a few hours prevented contracture formation.
In 1888, Petersen treated ischemic contracture by surgical release of contracted
muscles and scar tissue.11 He demonstrated some return of muscle function following this treatment. Seddon in 1964 reported that the process of skeletal muscle
13
regeneration after muscle ischemia in animals was observed by Kirby in 1892.55

Bunnell in 1948 and Harris in 1954 described the clinical entity and surgical
treatment of ischemic contracture of the hand.56,57
REFERENCES
1. Stenson, N.S., Elementorum myologiae specimen, seu musculi descriptio geometrica. Cui
accedunt canis carchariae dissectum caput, et dissectus piscis ex canum genere, Florentinae, Sub. signo. Stellae, 4, 123, 1667 (quoted by Haller: Elementa Physiol. 4, 544).
2. Hildebrand, O., Die Lehre von den ischemische Muskellahmungen und Kontrakturen,
Samml. Klin. Vortrage, 122, 437, 1906.
3. Severin, E., Umwandlung des musculus tibialis anterior in narbengewebe nach Uberanstrengung, 89, 427, 1943.
4. Vogt, P.R., Ischemic muscular necrosis following marching, read before the Oregon
State Medical Society, 1943 (cited by Horn, 1945).
5. Thomas, J.J., Nerve involvement in the ischemic paralysis and contracture of Volkmann, Ann. Surg., 49, 330, 1909.
289, 1973.
7. Volkmann, R., Ischaemic muscle paralyses and contractures, Clin. Orthop., 50, 5, 1881.
8. Lexsaser, E., Untersuchungen uber ischmischen Muskellahmungen und Muskelkontrakturen, Samml. Klin. Vortage, 249, 2087, 1884.
9. Hargens, A.R., Botte, M.J., Swenson, M.R., Gelberman, R.H., Rhoades, C.E., and
Akeson, W.H., Effects of local compression on peroneal nerve function in humans,
J. Orthop. Res., 11, 818, 1993.
10. Breit, G.A., Gross, J.H., Watenpaugh, D.E., Chanse, B., and Hargens, A.R., Nearinfrared spectroscopy for monitoring of tissue oxygenation of exercising skeletal
muscle in a chronic compartment syndrome model, J. Bone Jt. Surg., 79-A, 838, 1997.
11. Petersen, F., Uber ischmische Muskellahmungen, Arch. Klin. Chir., 37, 675, 1888.
12. Bernays, A.C., On ischemic paralysis and contractures of muscles, Bost. Med. Surg.
J., 542, 539, 1900.
13. Wallis, F.C., Treatment of paralysis and musclular atrophy after prolonged use of
splints or of an Esmarch's cord, Practitioner, 67, 429, 1901.
14. Littlewood, H., A clinical lecture on some complications following on injuries about
the elbow-joint and their treatment, The Lancet, 1, 290, 1900.
15. Murphy, J.B., Myositis, JAMA, 63, 1249, 1914.
16. Rorabeck, C.H., Macnab, I., and Wadell, J.P., Anterior tibial compartment syndrome:
a clinical and experimental review, Can. J. Surg., 15, 249, 1972.
17. Sheridan, G.W. and Matsen, F.A., An animal model of the compartmental syndrome,
Clin. Orthop., 113, 36, 1975.
18. Brooks, B., Pathologic changes in muscle as a result of disturbances of circulation:
an experimental study of Volkmann's ischemic paralysis, Arch. Surg., 5, 118, 1922.
19. Jepson, P.N., Ischaemic contracture: experimental study, Ann. Surg., 84, 785, 1926.
20. Styf, J.R. and Wiger, P., Abnormally increased intramuscular pressure in human legs:
comparison of two experimental models, J. Trau., 45, 133, 1998.
21. Wiger, P. and Styf, J.R., Effects of limb elevation on abnormally increased intramuscular pressure, blood perfusion pressure and foot sensation: an experimental study
in humans., J. Orthop. Trau., 12, 343, 1998.
14

22. Zang, Q., Styf, J., and Lindberg, L.-G., Effects of limb elevation on increased intramuscular pressure on human tibialis anterior muscle blood ow, Eur. J. Appl. Physiol.,
85, 567, 2001.
23. Bardenheuer, L., Die ischmische Kontraktur und Gangrn als folge der Arterienverletzung, Leutholds Gedenkschrift, 2, 87, 1906.
24. Leriche, R., Surgery of the sympathetic system: indications and results, Ann. Surg.,
88, 449, 1928.
25. Grifths, D.L., Volkmanns ischaemic contracture, Br. J. Surg., 28, 239, 1940.
26. Sirbu, C.A.B., Murphy, M.J., and White, A.S., Soft tissue complications of fractures
of the leg, West. Med., 60, 53, 1944.
27. Kinmonth, J.B., Simeone, F.A., and Perlow, V., Factors affecting the diameter of large
arteries with particular reference to traumatic spasm, Surgery, 26, 452, 1949.
28. Seddon, H.J., Volkmanns ischaemia in the lower limb, J. Bone Jt. Surg., 48-B, 627,
1966.
29. Gardner, R.C., Impending Volkmanns contracture following minor trauma to the
palm of the hand: a theory of pathogenesis, Clin. Orthop., 72, 261, 1970.
30. Willis, R.B. and Rorabeck, C.H., Treatment of compartment syndrome in children,
Orthop. Clin. N. Am., 21, 401, 1990.
Lancet, 19, 928, 1949.
32. Blandy, J.P. and Fuller, R., Ischemic myositis of the leg muscles from exercise, J.
Bone Jt. Surg., 39-B, 679, 1957.
33. Mavor, G.E., The anterior tibial syndrome, J. Bone Jt. Surg., 38-B, 513, 1956.
34. Grifths, D.L., The anterior tibial syndrome: a chronic form, J. Bone Jt. Surg., 38B, 438, 1956.
35. Grunwald, A. and Silberman, Z., Anterior tibial syndrome, JAMA, 171, 132, 1959.
37. Reneman, R.S., The anterior and lateral compartment syndrome of the leg, Ph.D.
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38. Landerer, A.S., Gewebspannung in ihrem Einuss auf die rtliche Blutbewegung
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39. Starling, E.H., On the absorption of uids from the connective tissue spaces, J.
Physiol. (Lond.), 19, 313, 1896.
40. Hendersson, Y., Oughterson, A.W., Greenberg, L.A., and Searle, C.P., Muscle tonus,
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41. Burch, G.E. and Sodeman, W.A., The estimation of the subcutaneous tissue pressure
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45. Rorabeck, C.H., Hardie, R., and Logan, J., Compartmental pressure measurements:
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46. Styf, J., Evaluation of injection techniques for recording of intra-muscular pressure,
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15
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Etiology and Pathogenesis

of Acute Compartment
Syndrome
INTRODUCTION
Acute compartment syndrome most often affects muscles contained in relatively

unyielding osteofascial spaces. The syndrome is more likely to evolve in round,
fusiform muscles than in flat, thin muscles with a thin epimysium. However, the
syndrome may evolve in any muscle as long as the tissue pressure is high enough
during a prolonged period of time.
The incidence is significantly higher in patients under 35 years of age. The
young patient with tibial diaphyseal fracture and the young male with a forearm
fracture sustained in high-energy trauma have increased risk for developing an acute
compartment syndrome.1,2
Pathogenesis of the syndrome is the abnormally increased intramuscular pressure within one or more well-defined osteofascial spaces. Abnormally increased
intramuscular pressure may be induced in several ways (Figure 3.1). The first
etiology is increased volume of the compartment contents. This is seen in patients
with hematoma, edema, or a combination of the two. The second etiology is prolonged ischemia of a limb with or without initial swelling. It may be due to external
compression, arterial occlusion, limb elevation, or to any combination thereof. The
third etiology is decreased size of the compartment, which may be induced by scar
formation following circumferential burn injuries. Finally, pathogenesis of an acute
compartment syndrome may include one or more of these etiologies simultaneously.
Knowledge about the etiology and pathogenesis of the syndrome is helpful to
diagnose and take measures to prevent the development of an imminent acute
compartment syndrome.
INCREASED VOLUME OF THE COMPARTMENT

CONTENTS
Hematoma, edema, or a combination of the two increases intramuscular pressure
because of increased volume of compartment contents (Table 3.1).
FRACTURES
Fractures are the most common reason for abnormally increased tissue pressure.
Thomas showed this in 1909.3 Fracture of the tibia may induce an acute compartment
17
18
Increased volume
of compartment
contents
Limb
elevation
Arterial
occlusion
External
compression
Decreased
compartment
size
Prolonged ischemia
Postischemic reperfusion
Abnormally increased intramuscular pressure
FIGURE 3.1 The possible mechanisms for pathogenesis of elevated intramuscular pressure
and acute compartment syndrome include increased volume of the compartment, prolonged
ischemia, and decreased size of the compartment, or any combination thereof.
syndrome in about 3 to 10% of the patients.47 The risk may be even higher in open
fractures.8 Compartment syndrome occurred in 20% of the children with fractures
of the midshaft of the radius and ulna.9 The syndrome may occur after reduction of
a displaced fracture.10 Intramuscular pressure increased by 7 mmHg when fractures
were reduced by traction. In another study, pressure increased an average of
12 mmHg when calcaneal traction was used.11
Transient increase in compartment pressure occurs during reaming of tibial
fractures.1215 Patients with associated head injuries have increased risks for sequel
from missed compartment syndrome.14 Therefore, intracompartmental pressure
should be measured in any patient with signs of elevated intramuscular pressure in
whom a reliable clinical examination cannot be performed. Both the duration and
magnitude of the elevated pressure must be considered.
Excessive traction of the lower limb is likely to increase the risk of compartment ischemia. Application of 6 kg of traction increased the mean resting
pressure by more than 30%.11 This may be explained by the sudden decrease in
the volume of the compartment when the relaxed soft tissues and bones suddenly
are distracted.
SOFT TISSUE TRAUMA

Ischemic contractures have been described following soft tissue injury alone.16
Permanent neuromuscular damage may also occur in patients with no or few clinical
symptoms.7 Closed muscle rupture is an uncommon cause for the syndrome.1719 It
has been described following peroneal muscle rupture in a rugby player and in the
forearm of a forestry worker.19 It has also been described in the thigh following
rupture of the vastus lateralis muscle.20
Etiology and Pathogenesis of Acute Compartment Syndrome
19
TABLE 3.1
Literature on Etiology and Pathogenesis of Acute Compartment
Syndromes: Increased Volume of Compartment Contentsa
Ref.
Bleeding
Fractures
Muscle rupture
Surgery
Arterial injury
6, 8, 10, 13, 14, 8791

1719, 92
41, 93 12, 15, 75, 94, 95
37, 9698
Edema
Venous stasis
Capillary leak syndrome
Exercise
Inflammation
51, 68, 99103

104107
24, 108, 109
110, 111
Bleeding and Edema
Fractures
4, 6, 7, 9, 10, 14, 87, 112122
Other Reasons for Volume Load

Intraosseus infusion
40, 123
Combined arterial and venous injuries
97
Dissecting popliteal cyst
124
Treatment by thrombolysis and coronary bypass
125, 126
Knee arthroscopy
127
Hip arthroplasty
4143
a
Increased volume of the compartment contents due to bleeding, edema, or a combination

of the two may increase intramuscular pressure to abnormal levels.
SURGICAL TREATMENT
The syndrome may develop in patients following surgical treatment by the Hauser
operation, proximal tibia osteotomy, and intramedullary nailing of the tibia.15,21,22
Postoperative hematoma may play a significant role in the development of acute
compartment syndrome. Patients treated by wound drainage following tibial osteotomy have significantly lower pressure in the anterior compartment compared to that
of patients without drainage.23
EXERCISE
Exercise-induced edema by marching and mountain climbing may be another reason
for acute compartment syndrome. In a review of literature, Bradley reported that in
one third of all patients with acute compartment syndromes, the conditions were
induced by exercise.24 Recent publications report that exercise is an uncommon
reason for acute compartment syndrome in the upper extremities,25,26 the thigh,27,28
leg,2932 and foot.33,34
20
OTHER REASONS
FOR INCREASED
VOLUME
Bleeding because of vascular injury and coagulopathy are other reasons for
hematoma.35 Also, intramuscular injections in patients who receive anticoagulation
treatment increase the risk for the syndrome to develop.36,37 Intravascular injections
may also induce acute compartment syndrome.36,38 Ischemic contracture was
described following arterial aneurysm of a fractured tibia.39 Intraosseos infusion
may induce the syndrome.40 The syndrome may follow in a swollen thigh after
total hip arthroplasty.4143
PROLONGED ISCHEMIA
The second etiology for increased intramuscular pressure is prolonged external
compression, arterial occlusion, limb elevation, or any combination thereof (Table
3.2). They may all induce a postischemic reperfusion injury to the capillary bed.
Tissue hypoxia induces dysfunction of the endothelial cells of the capillary bed,
which may leak plasma and water into the interstitial space. The reperfusion syndrome increases intramuscular pressure directly and by increased volume of the
interstitial space of the compartment contents.
EXTERNAL COMPRESSION
After prolonged ischemia due to external compression, a compartment syndrome
may occur due to postischemic swelling. Ischemia induces dysfunction of the endothelial cells, which leak plasma into the interstitial space following ischemic damage.4447 Six hours of external compression induced a reperfusion injury. About 50%
of the muscle fibers were damaged.48 However, distal muscles that were exposed to
TABLE 3.2
Syndromes: Prolonged Ischemiaa
Eternal Compression
Pneumatic antishock garments
Lumbar spine surgery
Tourniquet
External compression and limb elevation
Ref.
52, 5558, 71, 128, 129

130
131
61, 63, 69, 132
Arterial Occlusion
Arterial thrombosis
96, 133
External Compression and Limb Elevation

Prolonged surgery in the lithotomy position
51, 6165, 67, 68, 132, 134
a
Prolonged ischemia due to external compression, arterial occlusion, and limb elevation
may induce ischemia and a postischemic reperfusion syndrome.
21
Casted leg
Noncasted leg
Pressure
Volume
FIGURE 3.2 Schematic drawing of the relationship between volume and pressure in a compartment of a casted leg (dotted line) and noncasted leg (solid line).
ischemia but not to external compression did not demonstrate any increased damage
with reperfusion.
External compression by tight bandages such as orthoses, plaster cast, or elastic
stockings increases intramuscular pressure. A tight plaster cast decreases the compliance of compartment tissues.4951 A normal swelling of a limb may therefore create
pathologically increased intramuscular pressure (Figure 3.2).
Another reason for increased intramuscular pressure by external compression
is long-term unconsciousness in drug-addicted patients5254 and in patients treated
by military antishock trousers.5560 Figure 3.3 illustrates how intramuscular pressure
in the arm increases to high levels if it is compressed between the chest and a hard
undersurface.
External compression
FIGURE 3.3 The right arm of the subject exposed to external compression of a forearm.
22
Elevation
FIGURE 3.4 Elevated limbs in the lithotomy position decrease the leg perfusion pressure
significantly. The risk for acute ischemia is increased if the limb is elevated during an extended
period of time.
ARTERIAL OCCLUSION
Intramuscular pressure is initially normal in patients with total arterial occlusion.
Successful surgical treatment of arterial occlusion may induce a reperfusion injury of
the capillary bed. The time period for warm ischemia of extremity is important to
estimate and document. If it exceeds 6 hours of complete ischemia, the endothelial
cells most likely will be damaged and leak plasma into the interstitial space.44,48
LIMB ELEVATION
Patients with arteriosclerosis and diabetes of the lower limb have increased risks for
insufficient blood perfusion and development of ischemia. Acute compartment syndrome of the lower extremities has been described following colorectal surgery,61
urology (lithotomy position),6264 and pelvic surgery.65 Adverse effects in subjects
with an elevated limb and abnormally increased intramuscular pressure have been
described in experimental studies on humans (Figure 3.4).51,61,6670
DECREASED SIZE OF THE COMPARTMENT

The third etiology for increased tissue pressure is decreased volume of the compartment.
This may be due to closure of fascial defects and scar formation due to burn and frost
injuries (Table 3.3). Restricted swelling of a normally sized compartment may occur
in patients treated by plaster casts and other bandages after surgery and trauma.71,72
FASCIAL DEFECT
A fascial defect may be painful if the muscle tissue herniates through its opening.
This may occur during exercise when muscle tissue may swell up to 20% of its
initial volume. Acute compartment syndrome may occur following surgical repair
23
TABLE 3.3
Literature on Etiology and Pathogenesis of Acute
Compartment Syndromes: Decreased Size of the
Compartmenta
Closure of fascial defect
Burn injury
Ref.
20, 7375, 135139
52, 7679
Decreased size of the compartment increases intramuscular pressure

of the compartment tissues.
of symptomatic fascial defects.7375 Therefore, fascial defects must not be sutured.

They should be treated by fasciotomy through the defect. Patients with circumferent
injuries on the extremities may develop an inelastic scarring, which will prevent
normal volume increase of the underlying tissues.
BURN INJURY
In deep circumferential burns of an extremity, the skin loses its elasticity and
becomes relatively rigid. The constrictive effects of circumferential burns may cause
acute compartment syndromes,52,76,77 which may be relieved by long, linear incisions
through the skin along the axis of the extremity. About 10% of patients with burn
injuries require escharotomy.78 Most of these patients may need a fasciotomy as
well. The anterior tibial muscle may be necrotic in burn injuries of the leg.76 Acute
compartment syndrome is difficult to recognize because these patients usually have
multiple concurrent problems.79
OTHER ETIOLOGIES
Additional etiologies for acute compartment syndrome include prolonged anesthesia,80 different infections,81,82 and viper bite (Table 3.4).83 Excessive traction of the
lower limb is likely to increase the risk of compartment ischemia. Application of
6 kg of traction increased the mean resting pressure by more than 30%.11 This may
be explained by the sudden decrease in the volume of the compartment when the
relaxed soft tissues and bones are suddenly distracted. Viral infections may cause
rhabdomyolysis by direct cell injury or by toxin release.84,85 Rhabdomyolysis induced
by influenza infection leading to acute compartment syndrome has been described
in patients with severe myalgia.84,85 Patients with sickle cell trait have been reported
to suffer from acute compartment syndrome of the leg.86
SUMMARY
The etiology of acute compartment syndrome includes abnormally increased volume
of a compartment, prolonged ischemia, external compression, or any combination
24
TABLE 3.4
Syndromes: Combined Etiologies and Other Mechanisms
Etilogy and Pathogenesis
Ref.
Anesthesia
Local nerve block

Epidural anesthesia
Infection
114, 140
80, 141
81, 82, 85
Poisoning
Snake bite
Limb elevation
Drugs
83, 142
51, 6169, 99, 132, 134, 143145
5254
Combined etiologies and other mechanisms may increase intramuscular pressure to

abnormal levels.
thereof. The pathogenesis is abnormally increased intramuscular pressure, which

impedes the local muscle blood flow. Fractures, soft tissue trauma, surgical treatment,
and exercise may induce increased volume of the compartment. Prolonged external
compression, arterial occlusion, burn injuries, and limb elevation may create
ischemia. They may all induce a postischemic reperfusion injury to the capillary
bed. Tissue hypoxia induces dysfunction of the endothelial cells of the capillary bed,
which may leak plasma and water into the interstitial space. The reperfusion syndrome increases intramuscular pressure directly and by increased volume of the
interstitial space of the compartment contents. When released, these conditions may
induce a reperfusion injury to the endothelial cells of the capillary bed. The third
etiology is decreased compartment size following suture of fascial defects and
circumferent burn injuries. Other causes include prolonged anesthesia, infections,
viper bite, and any condition that causes rhabdomyolysis.
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Pathophysiology of
Acute Compartment
Syndrome
INTRODUCTION
One function of the local circulation is to deliver oxygen and to return waste products,
i.e., to maintain tissue nutrition and viability. In acute compartment syndrome, the
local circulation does not meet this demand. The pathophysiology of acute compartment syndrome describes the effects of increased compartment pressure on muscle
blood flow and muscle and nerve function. It describes how arterial pressure, venous
pressure, and perfusion pressure are affected by increased tissue pressure.
Tissue damage due to ischemia is directly related to microvascular perfusion.
Several mechanisms possibly act together in different clinical situations. The different mechanisms for regulation of local muscle blood flow may act together.
THEORIES ON LOCAL REGULATION OF MUSCLE

BLOOD FLOW
Understanding the pathophysiology of acute compartment syndrome is understanding the determinants of regional blood flow and how they are affected by increased
intramuscular pressure. Some authors have related tissue pressure to diastolic blood
pressure,1,2 whereas others have found the relationship between mean arterial blood
pressure and intramuscular pressure to better correlate with local perfusion pressure
and muscle viability.35 Theories on local regulation of muscle blood flow include
perfusion pressure, microvascular occlusion, critical closing pressure, tidal wave,
and arterial spasm.
PERFUSION PRESSURE
The arteriovenous gradient theory is based on the hydrodynamic principles described
in the law of Poiseuille:
Q = k r4 (P1 P2)/L N
(4.1)
where Q is the flow volume, K a constant (P/8), P1 P2 the pressure difference in

the direction of flow, r the radius of the vessel, L the length of the vessel, and N the
33
34
viscosity of the fluid. According to this law, the resistance (R) for blood flow is
given by:
R = 8L N
(4.2)
Therefore, muscle blood flow (MBF) in the arteriovenous gradient theory can be
expressed as:
MBF = (Pa Pv)/R
(4.3)
where Pa is the pressure at the arterial end and Pv the pressure at the venous end of
the capillary bed.
Mean arterial pressure (MAP) is a function of the systolic (S) and diastolic (D)
blood pressures. It is calculated by adding one third of the pulse pressure (S D)
to the diastolic blood pressure:
MAP = D + 1/3(S D)
(4.4)
Perfusion pressure (PP) is the difference between MAP and venous pressure (Pv) at
the end of the capillary (Figure 4.1):
PP = MAP Pv
(4.5)
Pressure
MAP
MAP
Perfusion pressure
Perfusion pressure
PV
Elevated IMP
PV
Normal
IMP
Normal intramuscular pressure
Normal
IMP
Elevated intramuscular pressure
FIGURE 4.1 Schematic illustration of the pathophysiology of acute compartment syndrome.

Intramuscular pressure (IMP) at rest is normally ca. 5 mmHg at heart level in the supine subject.
Perfusion pressure (PP), which is the difference between mean arterial pressure (MAP) and
intramuscular pressure, normally exceeds 70 mmHg (left). The elevated IMP decreases the local
PP as illustrated to the right. Redrawn after Matsen et al. (1980).33
Pathophysiology of Acute Compartment Syndrome
35
The pressure inside patent veins (Pv) can never be less than the extramural pressure.6,7
Increased intramuscular pressure decreases the arteriovenous pressure difference by
increasing the venous pressure (Pv). This leads to decreased PP. Therefore, intramuscular pressure (Pt) can be equal to venous pressure in Equation 4.3 and Equation
4.5. It has been shown that increased intramuscular pressure reduces the local
arteriovenous gradient and thereby reduces the local MBF810:
PP = MAP Pt
(4.6)
Local PP is a function of both MAP and local muscle pressure. By measuring intramuscular pressure, one can estimate PP because blood pressures are known. The overall
goal is to obtain a measure on the local PP. PP must exceed 40 mmHg in a traumatized
muscle and 30 mmHg in a normal muscle. Which level of intramuscular pressure a
patient can manage depends on the level of MAP and the position of the limb.
MICROVASCULAR OCCLUSION
According to the microvascular occlusion theory, an absolute compartment pressure
exists, which induces the syndrome.1113 Normal capillary pressure at rest is between
20 and 30 mmHg. The limiting factor in MBF disturbances has been shown to be
at the capillary level.5,11,14 Increased intramuscular pressure causes capillary vessels
to collapse at their distal end.15 This finding may be explained by the theory of
microvascular occlusion.
CRITICAL CLOSING PRESSURE

Burton first suggested the critical closing pressure theory in 1951.6 Evidence for this
concept was reported by Ashton in 1962,16 who showed that the positive pressure
intercept at zero blood flow was 33.4 (range 10 to 68) mmHg in the forearm of
normal subjects at rest (Figure 4.2). This means that MAP is 33 mmHg higher than
intramuscular pressure at zero blood flow.6,17 This was explained in terms of active
closure of the small arteries in muscle tissue.18 With this theory, it is possible to
explain the decrease of MBF when intramuscular pressure exceeds ca. 40 mmHg in
a normotensive subject. Active closure of small arterioles under vasomotor tone may
thus occur when the transmural pressure is lowered by decreased intravascular
pressure or increased tissue pressure. On the other hand, others have found no
evidence of a critical closing pressure by using nonpulsatile flow.19
The work by Heppenstall and co-workers also supports the critical closing
pressure theory. They showed that blood flow was a function of the difference
between MAP and intramuscular pressure in the compartment. When PP (Heppenstalls delta-p pressure) declined to below 30 mmHg, the requirements for normal
tissue viability were not fulfilled.20
TIDAL WAVE
With this theory, Dahn et al. explained the importance of diastolic blood pressure
for perfusion of the capillary bed in patients with hypotension.21 They found that
36
Blood flow
30 to 40 mmHg
Perfusion pressure
FIGURE 4.2 The critical closing pressure theory illustrates how muscle blood flow (MBF)
ceases to zero when the local PP is still between 30 and 40 mmHg.
MBF did not cease until external compression reached the systolic blood pressure
when venous stasis was used. They also found that MBF stopped when the locally
applied compression was equal to the diastolic blood pressure. The explanation for
this is given by the tidal wave theory or Starling valve theory,21 which postulates
that the microcirculation does not remain open long enough to allow perfusion
(Figure 4.3). The vascular bed is thought to collapse when the transmural pressure
falls to zero.
ARTERIAL SPASM
Increased intramuscular pressure and arterial injuries have been suggested to induce
arterial spasm.2224 The finding of normal pulses of the dorsal pedis artery of patients
with acute compartment syndrome does not support this theory.
Limb compartment
Heart
Artery
Collapsed vessel
Artery
FIGURE 4.3 Schematic illustration of the tidal wave theory. The microcirculation does not
remain open long enough during diastole to allow for blood flow. The elevated hydrostatic
pressure within the limb compartment forces the vessels to collapse during diastole. A transient
pressure increase during systole will only expand the left part of the vessel.
37
PATHOPHYSIOLOGY OF ABNORMALLY INCREASED

Despite distal pulses being palpable in patients with acute compartment syndrome,
local nutritive capillary blood flow may be compromised due to increased compartment pressure. The effects of increased intramuscular pressure on arterial blood
pressure, venous blood pressure, MBF, muscle oxygenation, and neuromuscular
function are discussed.
ARTERIAL BLOOD PRESSURE

MAP in the main arteries of the leg is unaffected by an inflated thigh tourniquet to
60 mmHg or by abnormally elevated intramuscular pressure to 40 mmHg in a casted
leg that was obstructed by venous stasis.9,25 Increased intramuscular pressure limits
flow mainly through increased critical closing pressure and with only a small change
in arterial resistance.26
VENOUS BLOOD PRESSURE

Venous pressure cannot be lower than the hydrostatic pressure of the surrounding
tissues.7,26 Therefore, increased tissue pressure induces a local venous hypertension, which decreases the local PP and blood flow according to Equation 4.3 and
Equation 4.5 (Figure 4.1). Increased intramuscular pressure that exceeds recumbent tibial vein pressure impairs flow in the tibial veins.27 There is a close relationship between abnormal venous blood flow and subsequent development of
neuromuscular deficit.
Venous hypertension is an important factor for the development of acute compartment syndrome in the lower limbs.2830 Jepson described the development of
acute compartment syndrome in the leg of dogs after venous obstruction of the dogs
leg. He concluded that contracture deformity depends on a combination of factors,
of which the impaired venous flow is the most important.31
MUSCLE BLOOD FLOW

Figure 4.4 summarizes the effects of increased intramuscular pressure on local MBF
by the different theories. The critical intramuscular pressure level that ceases local
MBF may vary significantly depending on the theory applied.
Factors that allow skeletal muscle to compensate to maintain adequate viability
include initial autoregulation of the microcirculation and enhanced venous oxygen
extraction. Autoregulation compensates for the decreased blood flow by decreasing
vascular resistance.
MUSCLE OXYGENATION
The ischemia-reperfusion injury triggers release of oxygen-derived free radicals
originating from endothelial cells. The injury is also aggravated by activation of
neutrophils producing free radicals. Neutrophils have also been found to contribute
38
BP 90/60 mmHg
MBF
A.
B.
30
40
E.
C.
50
D.
60
80 IMP
70
BP 120/80 mmHg
MBF
A.
30
B.
40
50
E.
60
C.
70
D.
80
IMP (mmHg)
FIGURE 4.4 Schematic curves describing the relationship between IMP and local MBF in
a subject with blood pressure of 90/60 mmHg (upper trace) and in another with blood pressure
of 120/80 mmHg (lower trace), according to the microvascular occlusion theory (A), critical
closing pressure theory (B), tidal wave theory (C), arteriovenous pressure gradient theory (D),
and the delta-p concept (E).
to microvascular dysfunction and abnormalities of blood flow distribution in experimental studies on acute compartment syndrome.32
Intramuscular oxygenation approaches zero when intramuscular pressure
reaches MAP locally.33 Endothelial cells of the capillary bed become dysfunctional,
allowing leakage of fluid and plasma proteins into the interstitial space.34 Increased
tissue pressure to between 40 and 60 mmHg impedes tissue oxygenation.8,35 Total
ischemia during 4 h damages 5% of the muscle cells. Total ischemia during 8 h
damages 100% of the muscle cells.2
NEUROMUSCULAR FUNCTION
Muscle function depends on the structural integrity of the muscle and on an intact
motor nerve and endplate. Once the local MBF is reduced to levels where it no
longer meets the metabolic demands of tissues, losses of tissue function and viability
ensue.33 Nerve conduction velocity decreases when intramuscular pressure reaches
40 to 60 mmHg.8,25,36,37
HYPOTENSION AND LIMB ELEVATION

The local MBF10 and PP9,25,33,38,39 are greatly influenced by limb position. Elevation
of extremity is commonly used to control bleeding in traumatized patients and
following limb surgery. Limb elevation after prolonged surgery may also provoke
acute compartment syndrome.4042 How arterial blood pressure, venous blood flow,
abnormally elevated interstitial hydrostatic pressure in the compartment, and
39
neuromuscular functions are affected by limb elevation is discussed in the following section.
ARTERIAL BLOOD PRESSURE

Mean arterial blood pressure and local PP decrease significantly by limb elevation.
Elevation of a limb with increased intramuscular pressure may induce symptoms of
imminent acute compartment syndrome.9 Studies have shown that elevating a limb
can impede local MBF.43,44 Hypotension of the central circulation due to hypovolemia
decreases MAP.
VENOUS RETURN
Venous stasis induces edema formation.45,46 Like venous hypertension, it can be an
important factor in the development of compartment syndrome in extremities.2831
Limb elevation has also been recommended as a treatment for patients with posttraumatic venous hypertension.47 Other factors that may decrease venous return from
the lower limbs are increased intraabdominal pressure,48,49 injuries to the pelvis,50
and extensive thrombosis.29,51
INTERSTITIAL HYDROSTATIC PRESSURE

Abnormally elevated intramuscular pressure in leg compartments does not
decrease significantly by limb elevation.8,9 However, moderate increase of intramuscular pressure due to vein obstruction alone is decreased by limb elevation.9
The combined effects of increased leg volume by venous obstruction and
restricted swelling by plaster cast increase compartment pressure more than what
would be expected by a simple summation of the pressures.8,9,52 The phenomenon
of amplification and summation of intramuscular pressure in an obstructed and
casted leg has been described in animal experiments8,52 as well as in human
studies.9,53
NEUROMUSCULAR FUNCTION
Intramuscular pressure levels exceeding 35 mmHg combined with limb elevation
have been shown to decrease PP to levels that induce neuromuscular dysfunction.9,33
When intramuscular pressure reaches 40 mmHg in a casted elevated leg with venous
obstruction, subjects experience gradual loss of sensation in the foot or throbbing
discomfort (Figure 4.5).
SUMMARY
Pathophysiology of acute compartment syndrome is the study of how abnormally
elevated intramuscular pressure affects the function of blood flow, muscle, and nerve.
Local PP is important to calculate in patients having impending acute compartment
syndrome. PP is a function of the difference between MAP and intramuscular
pressure at rest. Venous hypertension is an important factor for development of the
40
FIGURE 4.5 An experimental model to study the pathophysiology of elevated intramuscular

pressure and limb elevation. Blood pressures are measured in the distal part of both limbs
and in the upper arm. Venous stasis is applied by thigh tourniquet (60 mmHg). Both legs are
casted; one leg is elevated.
syndrome. Limb elevation decreases mean arterial blood pressure. Tissue hydrostatic
pressure and local venous pressure are unaffected by limb elevation.
REFERENCES
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Determination of the compartment pressure threshold of muscle ischemia in a canine
model, J. Trau., 37, 50, 1994.
2. Whitesides, T.E., The response of skeletal muscle to temporary ischemia: an experimental study, J. Bone Jt. Surg., 53-A, 1026, 1971.
3. Heppenstall, R.B., Scott, R., Sapega, A., Park, Y.S., and Chance, B., A comparative
study of the tolerance of skeletal muscle to ischemia, J. Bone Jt. Surg., 68-A, 820,
1986.
4. Heppenstall, R.B., Sapega, A.A., Scott, R., Shenton, D., Park, Y.S., Maris, J. et al.,
The compartment syndrome: an experimental and clinical study of muscular energy
metabolism using phosphorus nuclear magnetic resonance spectroscopy, Clin.
Orthop., 226, 138, 1988.
5. Reneman, R.S., Slaaf, D.W., Lindblom, L., Tangelder, G.J., and Arfors, K.E., Muscle
blood flow disturbances produced by simultaneously elevated venous and total muscle
tissue pressure, Microvasc. Res., 20, 307, 1980.
6. Burton, A.C. and Yamada, S., Relation between blood pressure and flow in the human
forearm, J. Appl. Physiol., 4, 329, 1951.
7. Kjellmer, I., An indirect method for estmating tissue pressure with special reference
to tissue pressure in muscle during exercise, Acta Physiol. Scand., 62, 31, 1964.
8. Matsen, F.A., King, R.V., Krugmire, R.B., Mowery, C.A., and Roche, T., Physiological effects of increased tissue pressure, Int. Orthop., 3, 237, 1979.
41
10. Zang, Q., Styf, J., and Lindberg, L.-G., Effects of limb elevation on increased intramuscular pressure on human tibialis anterior muscle blood flow, Eur. J. Appl. Physiol.,
85, 567, 2001.
11. Hargens, A.R., Akeson, W.H., Mubarak, S.J., Owen, C.A., Evans, K.L., Garetto, L.P.,
Gonsalves, M.R., and Schmidt, D.A., Fluid balance within the canine antero-lateral
compartment and its relationship to compartment syndromes, J. Bone Jt. Surg., 60A, 499, 1978.
12. Hargens, A.R., Schmidt, D.A., Evans, K.L., Gonsalves, M.R., Cologen, J.B., Garfin,
S.R. et al., Quantitation of skeletal muscle necrosis in a model compartment syndrome, J. Bone Jt. Surg., 63-A, 631, 1981.
13. Mubarak, S.J., Owen, C.A., Hargens, A.R., Garetto, L.P., and Akeson, W.H., Acute
compartment syndromes diagnosis and treatment with the aid of the wick, J. Bone
Jt. Surg., 60-A, 1091, 1978.
14. Hargens, A.R., Mubarak, S.J., Owen, C.A., Garetto, L.P., and Akeson, W.H., Interstitial fluid pressure in muscle and compartment syndromes in man, Microvasc. Res.,
14, 1, 1977.
15. Beer, G., Role of tissue fluid in blood flow regulation, Circ. Res., 28/29 (suppl. 1),
154, 1971.
16. Ashton, H., Critical closing pressure in human peripheral vascular bed, Clin. Sci.,
22, 79, 1962.
17. Magder, S., Starling resistor versus compliance: which explains the zero flow pressure
of a dynamic arterial pressure-flow relation? Circ. Res., 67, 209, 1990.
18. Ashton, H., The effect of increased tissue pressure on blood flow, Clin. Orthop. Rel.
Res., 113, 15, 1975.
19. Folkow, B. and Lfwing, B., The distensibility of the systematic resistance blood
vessels, Acta Phys. Scand., 38, 37, 1956.
20. Heppenstall, R.B., Sapega, A.A., Izant, T., Fallon, R., Shenton, D., Park, Y.S. et al.,
Compartment syndrome: a quantitative study of high-energy phosphorus compounds
using 31P-magnetic resonance spectroscopy, J. Trau., 29, 1113, 1989.
21. Dahn, I., Lassen, N.A., and Westling, H., Blood flow in human muscles during
external pressure or venous stasis, Clin. Sci., 32, 467, 1967.
22. Eastcott, H.H.G., The management of arterial injuries, J. Bone Jt. Surg., 47-B, 394,
1965.
23. Gardner, R.C., Impending Volkmanns contracture following minor trauma to the
palm of the hand: a theory of pathogenesis, Clin. Orthop., 72, 261, 1970.
24. Griffiths, D.L., Volkmanns ischaemic contracture, Br. J. Surg., 28, 239, 1940.
Physiol., 83, 84, 2000.
26. Shrier, I. and Magder, S., Pressure-flow relationship in in vivo model of compartment
syndrome, J. Appl. Physiol., 79, 214, 1995.
27. Jones, W.G., Perry, M.O., and Bush, H.L., Changes in tibial venous blood flow in
the evolving compartment syndrome, Arch. Surg., 124, 801, 1989.
28. Kunkel, J.M., Thigh and leg compartment syndrome in the absence of lower extremity
trauma following MAST application, Am. J. Emerg. Med., 5, 118, 1987.
Surgery, 95, 191, 1984.
42

158, 136, 1989.
32. Sadasivan, K., Carden, D., Moore, M., and Korthuis, R., Neutrophil mediated
microvascular injury in acute, experimental compartment syndrome, Clin. Orthop.,
339, 206, 1997.
34. Mabee, J.R. and Bostwick, L., Pathophysiology and mechanisms of compartment
syndrome, Orthop. Rev., 22, 175, 1993.
35. Hargens, A.R., Romine, J.S., Sipe, J.C., Evans, K.L., Mubarak, S.J., and Akeson,
W.H., Peripheral nerve-conduction block by high muscle compartment pressure, J.
Bone Jt. Surg., 61-A, 192, 1979.
36. Gelberman, R.H., Szabo, R.M., Williams, R.V., Yaru, A.R.H.N.C., and MinteerConvery, M.A., Tissue pressure threshold for peripheral nerve viability, Clin. Orthop.,
178, 285, 1983.
J. Orthop. Res., 11, 818, 1993.
38. Chidgey, L.K., Szabo, R.M., and Kolack, B., Effects of elevation on nerve function
in an acute upper extremity nerve compression model, J. Orthop. Res., 7, 783, 1989.
1979.
Dis., 5, 1, 1990.
43. Ashton, H., Effect of inflatable plastic splints on blood flow, Br. Med. J., 2, 1427, 1966.
44. Matsen, F.A., Mayo, K.A., Krugmire, R.B., Sheridan, G.W., and Kraft, G.H., A model
compartmental syndrome in man with particular reference to the quantification of
nerve function, J. Bone Jt. Surg., 59-A, 648, 1977.
45. Aukland, K. and Nicolaysen, G., Interstitial fluid volume: local regulatory mechanisms, Physiol. Rev., 61, 556, 1981.
46. Fadnes, H.O., Effects of increased venous pressure on the hydrostatic and colloidosmotic pressure in subcutaneous interstitial fluid in rats: edema preventing mechanisms, Scand. J. Clin. Lab Invest., 36, 371, 1976.
48. Rubinson, R.M., Vasko, J.S., Doppman, J.L., and Morrow, A.G., Inferior vena caval
obstruction from increased intra-abdominal pressure: experimental hemodynamics
and angiographic observations, Arch. Surg., 94, 766, 1967.
43
50. Jacques, T. and Lee, R., Improvement of renal function after relief of raised intraabdominal pressure due to traumatic retroperitoneal hematoma, Anaesth. Intens. Care,
16, 478, 1988.
51. Saffle, J.R., Maxwell, J.G., Warden, G.D., Jolley, S.G., and Lawrence, P.F., Measurement of intramuscular pressure in the management of massive venous occlusion,
Surgery, 89, 394, 1981.
52. Garfin, S.R., Mubarak, S.J., Evans, K.L., Hargens, A.R., and Akeson, W.H., Quantification of intracompartmental pressure and volume under plaster casts, J Bone Jt.
Surg., 63-A, 449, 1981.
Diagnosis of Acute
Compartment Syndrome
INTRODUCTION
Acute compartment syndrome is dened as a condition in which increased interstitial

uid hydrostatic pressure impedes local muscle blood ow and impairs the function
of the tissues within a dened osteofascial space.1 Therefore, in the clinical situation,
one should search for signs of increased pressure, decreased blood ow, and impaired
function of muscles. The patients history and the physicians ndings at physical
examination are the cornerstones in diagnosing acute compartment syndrome.
Knowledge of pathophysiology, anatomic compartments, and the nerves passing
through them is essential for diagnosing the syndrome.
STAGES OF ACUTE COMPARTMENT SYNDROME

Development of the syndrome may be described in three clinical stages that are
related to pathophysiological stages. Stage I is abnormally increased intramuscular
pressure. Stage II is inadequate blood perfusion pressure of the compartment. Stage
III is impaired function of the muscles and nerves in the compartment (Figure 5.1).
Therefore, knowledge of the pathogenesis and pathophysiology of acute compartment syndrome is important to accurately diagnose the condition.
When a patients symptoms and signs elicited have reached Stage III, clinical
diagnosis may be easy to make. However, waiting for all the symptoms to develop
might jeopardize the viability of tissues in the compartment. Patients may lose
function permanently if the syndrome is treated after neuromuscular dysfunction
has occurred.2 A study found that only 15% of patients who experience neuromuscular dysfunction at the time of diagnosis regained normal function after treatment.3
Time duration is therefore an important factor. Furthermore, in multiply traumatized
patients, it may be difcult to differentiate between dysfunction induced by abnormally increased intramuscular pressure and dysfunction due to nerve injury. The
duration of each stage may vary considerably among patients.
SYMPTOMS AND SIGNS OF INCREASED INTRAMUSCULAR PRESSURE (STAGE I)

History
Patients with abnormally increased intramuscular pressure complain of tightness of
the compartment(s) and local pain. The duration of external compression is important
to investigate. It may be helpful to ask relatives or paramedics in which position the
unconscious patient was found. This helps focus on the affected compartments.
45
46
Stage
Pathophysiology
Clinical Symptoms
Increased intramuscular pressure
Swelling
Decreased range of motion
II
Decreased muscle
blood flow
Ischemic pain at rest

Pain at passive stretch
III
Impaired function
Sensory and motor

dysfunction
FIGURE 5.1 Three stages of the relationship between intracompartmental pathophysiology

and clinical symptoms.
Following external compression as well as successful surgical treatment for arterial

occlusion, the limb may initially appear normal. The swelling evolves over time.
Physical Examination
At examination the limb is swollen. Often the skin may reveal erythema over the
compressed area. The compartment is tense, tender, and painful at palpation. Usually,
there is no subcutaneous pitting edema in acute cases but the skin over the compartment may have a waxy or shiny character. Repeated measurements of the largest
circumference over the muscle belly of both limbs with a tape measure are helpful
to estimate the magnitude and speed of swelling. The site of measurement should
be marked on the skin. The passive range of motion of the joints over which the
compartment muscles act should be measured. The range of motion is often
decreased before passive stretch of the muscle becomes painful. Findings should be
compared with those in the contralateral extremity. The date and hour of the investigation must be documented in the patients le.
In rare cases, the limb may be extremely swollen and the tissues hard at
palpation, but the patient still has no pain. This is a time for close observation of
the patient, who may start to experience pain within a short period of time. Intramuscular pressure should be measured if the ndings are nonconclusive.
SYMPTOMS AND SIGNS OF INADEQUATE LOCAL TISSUE PERFUSION (STAGE II)

History
At this stage of the syndrome the patient complains of severe increasing pain. The
pain intensity is often out of proportion and is sometimes difcult to relate to the
primary injury or diagnosis. When the patients pain does not respond to analgesic
medication, the pathophysiological process may have induced tissue ischemia. The
patients lack of responsiveness to pain medication may sometimes be frustrating
Diagnosis of Acute Compartment Syndrome
47
for the medical staff. The patients pain may be very intensive and the objective
signs discrete. Some patients with ischemic pain experience and express severe
anxiety. This may sometimes interfere with normal pain behavior. We must not
primarily blame psychological factors or a low threshold for pain tolerance when
patients are experiencing pain with few objective signs for imminent acute compartment syndrome.
Physical Examination
The limb circumference increases further. Affected muscles are weak. The intensity
of pain increases momentarily when compartment muscles are exposed to passive
stretch. The reason for this is increased intramuscular pressure during passive stretch
of a muscle.4 Pressure in a volume-loaded compartment increases more during passive
stretch of a muscle than in a normally hydrated compartment (Figure 5.2). The range
of passive motion of the joint over which the muscle(s) function decreases with an
increase in compartment volume. Distal pulses are usually normal. Pressure in the
compartment is usually not high enough to affect ow in the main arteries. When
pulselessness occurs, it is a sign of arterial injury and not an acute compartment
syndrome. However, following arterial repair, a reperfusion syndrome may develop
if the time for warm ischemia is long enough. Warm ischemia is dened as nonow
in a limb with normal or near-normal body temperature. It is most helpful to document
the time period for warm ischemia in managing these patients. If the time period for
warm ischemia exceeds 4 to 6 h, most patients require treatment by fasciotomy.
Swelling
Sensory dysfunction
Normal pulses
Paresis
Pain at passive plantar flexion
FIGURE 5.2 Clinical ndings in patients with acute anterior compartment syndrome of the
leg. These patients have calf pain at passive exion of the ankle joint and the big toe.
48
SYMPTOMS
AND
SIGNS
OF
NEUROMUSCULAR DYSFUNCTION (STAGE III)
The duration of abnormally increased intramuscular pressure is as important as the

magnitude of pressure elevation in producing neuromuscular dysfunction.
History
At this stage, the patient experiences loss of sensation over the skin, which is
innervated by nerves that pass through the compartment. The patient complains of
muscular weakness or even inability to move the joints actively. The patient cannot
dorsiex the ankle joint if the anterior leg compartment is involved nor ex his/her
ngers if the volar compartment of the forearm is involved.
Physical Investigation
The patient is unable to activate the muscles of the compartment and has lost
sensation for light touch. Passive range of motion of the involved joint decreases
further. Compartment muscles are non-responsive to electrical stimulation.
LOCATION OF ACUTE COMPARTMENT SYNDROMES

The following sections present specic etiology and diagnosis of the syndrome in
the leg, foot, thigh, gluteal region, lumbar spine, shoulder, upper arm, forearm, and
the hand. The symptoms of Stage II and Stage III in different locations of acute
compartment syndrome are elucidated. In many patients, several compartments
within a limb may be involved. Therefore, symptoms from different locations often
may merge together. One example of this is the concurrent compartment syndromes
of the foot and leg after trauma.5
LEG COMPARTMENTS
The leg is the most common location for acute compartment syndrome.
Anatomy
The leg contains at least four separate osteofascial compartments (Figure 5.3).
The anterior compartment encloses the extensor muscles of the leg and the deep
peroneal nerve. It is one of the most nonyielding compartments. The tibialis
anterior muscle has an end artery supply, which makes it more vulnerable than
the other leg compartments. The lateral compartment contains the peroneal
muscles and the supercial peroneal nerve. The deep, posterior compartment
contains the ankle joint exors and toe exors as well as the tibialis nerve. The
existence of additional compartments is a matter of controversy. The supercial
posterior compartment consists of the medial and lateral gastrocnemius muscles
and the soleus muscle.
49
Anterior compartment
Deep posterior compartment
Lateral compartment
Superficial posterior compartment
FIGURE 5.3 The four or ve compartments of the leg. Some authors believe the tibialis
posterior muscle is located in a separate fth compartment.
Etiology
Fractures are the most common cause of the syndrome. The syndrome has been
reported to occur in 3 to 12% of all tibia fractures. Other causes for acute compartment syndrome are discussed in Chapter 3.
Clinical Findings in the Anterior Compartment of the Leg
The leg is swollen and tender lateral to the anterior margin of the tibia. The patients
pain intensity in the anterior compartment increases by passive plantar exion of
the ankle joint and the big toe. Skin sensation is lost over the rst interdigital cleft
and the patient develops a weak dorsiexion of the big toe and the ankle joint because
the deep peroneal nerve is affected in the anterior compartment (Figure 5.2).
Clinical Findings in the Lateral Compartment of the Leg
The lateral compartment is located in a proximodistal direction between the
bular head and the lateral malleolus (Figure 5.4). It is swollen and tender. By
passive supination of the ankle joint by the investigator, the patient experiences
increased pain intensity from the lateral compartment. Skin sensation is lost over
the dorsum of the foot because the supercial peroneal nerve is compressed in
the lateral compartment. Often both the anterior and lateral compartments are
involved and the patient develops a drop foot. The condition occurs most often
together with acute anterior compartment syndrome. Isolated peroneal compartment syndromes are unusual.6
50
Swelling
Pain at
passive supination
Drop foot
Sensory dysfunction
FIGURE 5.4 Symptoms and ndings of acute compartment syndrome in the lateral compartment.
Clinical Findings from the Posterior Compartments of the Leg

The calf is swollen and hard at palpation. By passive dorsiexion of the ankle
joint and toes by the investigator, the patient experiences increased pain intensity
from the muscles in the deep and supercial posterior compartments (Figure
5.5). The test is performed in a similar way as the Hohmans test for calf
thrombosis. During this test, the patient experiences increased pain intensity
from the muscles in the posterior compartments when the investigator passively
dorsiexes the ankle joint by pushing the sole of the foot. Skin sensation is lost
over the sole of the foot. The ability to grip the investigators index nger by
exing the toes is weak as well as the strength for plantar exion of the ankle
joint (Figure 5.2).
FOOT COMPARTMENTS
Acute compartment syndrome of the foot usually follows fractures and massive soft
tissue trauma to the foot. Early diagnosis and decompression are as important as in
other compartments to prevent loss of neuromuscular function.
Anatomy
Nine anatomical compartments in the foot have been identied:7 medial, supercial, lateral, adductor, the four interossei, and the calcaneal compartment. The rst
three compartments are divided into three main compartments by a medial and a
lateral intermuscular septum that run the entire length of the foot. The adductor
and the four interossei compartments are located in the forefoot, and the calcaneal
51
Swelling
Normal pulses
Pain at passive dorsiflexion
Sensory dysfunction
Weak plantar flexion
FIGURE 5.5 Symptoms and ndings of acute compartment syndrome in the posterior compartments.
compartment is located in the hindfoot.7 The neurovascular bundle runs through

the calcaneal compartment. This may explain some of the confusion regarding
reports on descriptions of compartment location in the foot. Some compartments
are found only in the forefoot, others in the hindfoot, and only a few of them are
located along the whole foot (Figure 5.6). The previously described central compartment is divided by a transverse fascia in the hindfoot into a supercial and
deep compartment.
Etiology
Crush injuries to the foot may induce acute compartment syndrome of the intrinsic
muscles.811 About 10% of patients with calcaneal fractures may develop elevated
hydrostatic pressure in the foot,11 and about half of these patients (5%) develop
claw-toes11 if left untreated. The syndrome may follow distortion of the foot.12
52
Interossei
Medial
Lateral
Central
FIGURE 5.6 Cross section of the midfoot. Nine different compartments exist. The calcaneus
compartment is located more dorsally toward the calcaneus bone.
Clinical Findings
In clinical diagnosis, it is difcult to separate the involvement of each compartment.
Therefore, different clinical ndings may not be related to a specic compartment
of the foot. The patient has a tense swelling in the arch of the foot, which is tender
to palpation. The patient may experience numbness and a tingling sensation in the
whole foot.
Pain on passive dorsiexion of the toes may indicate ischemia in the intrinsic
muscles of the foot.9,1315 It is the most reliable clinical nding and occurs in 86%
of patients.16 The sign is difcult to interpret, because in many patients this occurs
up to 22 months following surgical treatment. Objective motor decits and loss of
pinprick sensation is also difcult to estimate. Patients with crush injuries of the
foot may have cyanotic toes and delayed capillary lling time. The end results of
an untreated acute compartment syndrome in the foot are a painful dysfunctional
extremity with sensory disturbances, stiffness, contracture of the forefoot, and clawing of the toes.
THIGH COMPARTMENTS
Acute compartment syndrome in the thigh is a rare condition that can be seen in
patients with femoral fractures, crush injuries that develop into crush syndrome, and
severe contusion of the anterior thigh in contact sports.
Anatomy
The thigh has three compartments: anterior, posterior, and medial. They are separated by the lateral, posterior, and medial intermuscular septa, respectively (Figure
5.7). The anterior compartment includes the quadriceps muscles and the posterior
53
Quadriceps compartment
Adductor compartment
Posterior or hamstring compartment
FIGURE 5.7 Cross section of the thigh compartments. The medial compartment encloses
the adductor muscles. The vastus medialis obliquus, the rectus femoris, intermedius, and
vastus lateralis muscles comprise the quadriceps muscles. The hamstring muscles are located
in the posterior compartment.
compartment includes the hamstring muscles. The medial, or adductor, compartment contains the adductor muscles. Sensory distribution of the femoral nerve
includes lateral, intermediate, and medial cutaneous nerves of the thigh. The
saphenous nerve includes the sensory distribution over the medial parts of the
knee and leg.
Etiology
Thigh compartment syndromes may be seen in patients with multiple trauma,17
thigh contusion during athletic activity,1820 reperfusion syndrome following external compression, vascular injury, extensive venous thrombosis,21 and femur fractures.22 Many of the patients are multiply injured by high-energy trauma to the
thigh23 with or without femur fracture. The syndrome may follow external compression of the thigh by antishock trousers.24 It has been reported in patients with
systemic hypotension, coagulopathy, and vascular injury. In rare cases, it may be
induced by exercise.2527
Clinical Findings
The patient complains of intensive thigh pain. The thigh is swollen and tense. The
thigh circumference should be measured every hour initially. Sensory function of
the femoral nerve branches and the sciatic nerve may be impaired. The anterior
compartment is tested by passive exion of the knee joint while maintaining the hip
in neutral position. This is a sensitive test for increased volume of quadriceps muscles
in the anterior compartment. Pain on passive stretching of the muscles in the posterior
54
compartment is tested for by passively extending the knee joint while holding the
hip in 60 of exion. Even if only one of the compartments is involved initially,
other compartments are often affected reactively.
GLUTEAL COMPARTMENTS
Early diagnosis of gluteal compartment syndrome is difcult because it is rare and
poorly understood. It is important to diagnose the syndrome because the compartments
contain large muscle volumes, which may induce massive myoglobulinemi and the
crush syndrome. Gluteal compartment syndrome, although a rare condition, should be
included in the differential diagnosis of acute posttraumatic sciatic nerve palsy.
Anatomy
The pelvic region can be divided into four muscular compartments: (1) the iliopsoas muscle compartment, (2) gluteus medius and minimus, (3) gluteus maximus,
and (4) the anterolateral compartment with the tensor fasciae lata muscle.28 The
iliopsoas muscles lie in an osteofascial compartment consisting of the iliac bone
and the iliac fascia. The femoral nerve runs diagonally through the lateral border
of the psoas belly. The external rotators of the hip may induce neuromuscular
dysfunction by compressing the sciatic and peroneus nerves. At this level, the
peroneus nerve runs separately in almost 30% of the population. It may be difcult
to differentiate between nerve compression (entrapment) and compartment syndrome in trauma cases.
Etiology
Gluteal compartment syndromes have been reported following trauma in 15% of
patients,2831 prolonged external compression in drug-induced coma in 50% of
patients,3033 reperfusion syndrome following vascular surgery and positioning during other surgical procedures in 25% of patients,3032,34,35 and other disease-associated
conditions.31,36,37 Gluteal contractures have been reported in children following
numerous injections of antibiotics in the gluteal region.
Clinical Findings
Gluteal muscles are swollen and hard at palpation. The gluteal skin is red in patients
with long-term external compression. Any passive hip motion is painful, especially
exion and adduction. The proximity to the sciatic nerve can induce neuropathy by
compression. Leg and foot sensation may decrease. Patients may experience weakness in all lower extremity muscles and the Achilles reex may be absent. Dysfunction of the femoral nerve may lead to paralysis of the rectus femoris muscle and
loss of sensation in the distal anterior thigh as well as the anteromedial aspect of
the leg all the way to the medial malleolus.28 Later in the presentation of the disease,
patients may demonstrate dysfunction of the femoral and sciatic nerves by decits
in the thigh, leg, and foot strength. Sciatic nerve palsy caused by direct contusion
is unlikely to give the delayed onset of neuromuscular dysfunction. Most patients
55
Processus spinosus
Skin
Dorsolumbar
compartment
Vertebra
FIGURE 5.8 The dorsolumbar compartments are enclosed in unyielding osteofascial spaces.
have severe elevation of myoglobin in plasma and urine, and elevated plasma creatininphosphokinase (CPK).
LUMBAR PARASPINAL COMPARTMENTS

Anatomy
Based on anatomical dissection of the spine, a lumbodorsal compartment has been
suggested.38,39 The erector spinae muscles are located in unyielding osteofascial
space bounded anteriorly by the transverse processes and intertransverse ligaments.
The lumbodorsal fascia in the dorsal and lateral direction covers the compartments.
It is covered medially by both the laminae and the spinal processes with their
interconnecting ligaments (Figure 5.8).
Etiology
Acute compartment syndrome in the erector spine muscles and pain in the rectus
abdominis muscles was initiated by downhill skiing in one patient.40
Clinical Findings
The lumbar paraspinal muscles are rigid and tender. The lumbar lordosis is attened
and the lumbar spine exed. Straight-leg raising aggravates the back pain. Sensation
may be diminished over the lumbosacral area but not in the caudal area.40 In a
biomechanical study, the spinal exion combined with lordotic attening was labeled
as Bourbon tube effect.41
56
Trapezius muscle
Skin
Fascia
Scapular bone
Supraspinatus muscle
FIGURE 5.9 The supraspinatus muscle is located in an osteofascial space on the scapula,
underneath the trapezius muscle.
SHOULDER COMPARTMENTS
Anatomy
Four separate osteofascial compartments may be identied in the shoulder. These
are the three muscles related to the scapula,42 the supraspinatus, infraspinatus, and
the subscapularis muscles; the fourth is the deltoid muscle (Figure 5.9).
Etiology
Prolonged external compression in drug addicts and severe trauma to the scapula
may induce abnormally elevated intramuscular pressure in the muscles. Vigorous
exercise by bayonet fencing training induced symptoms of acute compartment syndrome in the supraspinatus muscle.43
Clinical Findings
Local triangular swelling proximal and distal of spinae scapulae indicates the
syndrome.42 Passive inward and outward rotation of the shoulder may induce
increased pain intensity due to increased pressure in the supraspinatus and
infraspinatus muscles.
UPPER ARM COMPARTMENTS

Anatomy
The upper arm has two compartments: the anterior compartment encloses the
biceps muscle, and the posterior compartment encloses the triceps muscle. On the
medial side between the compartments, the neurovascular bundle is located in the
57
Posterior compartment
FIGURE 5.10 Cross section of the anterior and posterior compartments of the upper arm.
The main neurovascular bundle runs medially between the compartments.
intermuscular septum (Figure 5.10). The fascial boundaries are not as rigid compared to the forearm and leg compartments.
Etiology
Direct trauma or compression of the upper arm in unconscious patients initiate the
syndrome.4448 It may follow as a complication of an inated pneumatic tourniquet,49
angiography, dislocation of the shoulder, and avulsion of the triceps surae muscle.50
Clinical Findings
Patients experience pain, swelling, and tenderness of the upper arm. Passive exion
or extension of the elbow induces severe pain, and the range of motion decreases
when the syndrome evolves. Sensation and grip strength of the hand may be reduced
due to dysfunction of the median nerve.49 The skin may show delayed capillary rell.
FOREARM COMPARTMENTS
Anatomy
The three major compartments in the forearm are the deep volar, supercial volar,
and dorsal. The extensor indices proprius muscle may be located in a separate fourth
compartment (Figure 5.11).
Etiology
The syndrome is described after forearm fractures,5154 cannulation of arm vessels,5557 and prolonged external compression. Between 2% and 3% of all forearm
58
Radius bone
Extensor compartment
Deep flexor
compartment
Ulnar bone
Superficial flexor
compartment
FIGURE 5.11 Cross section of the forearm showing an extensor compartment and two exor
compartments.
fractures develop a compartment syndrome.54 The etiology of forearm compartment

syndrome is injection of drugs in 30%, trauma in 40%, and external compression
of the arm in 15%. Less usual etiologies are severe burn injuries and diseases.
Thompkins presented a patient with exercise-induced acute compartment syndrome
in the forearm extensor compartment following strenuous canoeing.58
Clinical Findings
The muscles of the forearm are swollen and tender at palpation. Passive extension
of the ngers and the wrist induces severe pain in the volar compartments, and
patients may experience weakness of the handgrip. Patients may lose sensation in
their ngertips. Passive exion of the ngers and the wrist induces pain if the dorsal
compartment is involved.
HAND COMPARTMENTS
About half of the patients with acute hand compartment syndrome also have a
simultaneous forearm compartment syndrome.59 This implies that hand ischemia is
only one facet of a more complex clinical picture.
Anatomy
The ten compartments of the hand include the four dorsal interossei compartments; the
three volar interossei compartments; and the hypothenar, thenar, and adductor pollicis
muscle compartments (Figure 5.12). The carpal canal is also a physiologic compartment.
Edema and swelling within this space are bound by synovial tissue and cannot escape
proximally or distally. Some physicians consider six compartments of the hand.
59
Thenar
Hypothenar
Carpal tunnel
Adductor pollicis
Dorsal interossei (four)

Volar interossei (three)
FIGURE 5.12 Cross section through the carpal tunnel and the ten compartments of the hand.
Etiology
The etiology includes multiple fractures and snakebites,59 crush injuries, burn injuries,60 and intravenous and intraarterial injections.56,57
Clinical Findings
The patient has a painful, tense, and swollen hand. The metacarpophalangeal joints
are held extended and the interphalangeal joints exed. In this position, the interossei
muscles are short. The pain intensity increases by passive stretching of the involved
intrinsic muscles.61 However, in many cases, pain cannot be elicited by passive
motion of the ngers when only the hand is involved.59,61 Sensation in the digits is
usually normal. Later, and in more extensive cases, compression of the median nerve
results in sensory loss.
ADDITIONAL DIAGNOSTIC TOOLS

Diagnosis by clinical examination is sometimes easy and conclusive. However, it requires
a conscious patient who can cooperate and an experienced examiner. Therefore, adjunctive diagnostic techniques such as bedside measurements of intramuscular pressure or
direct noninvasive nerve stimulation may be helpful diagnostic tools. Other noninvasive
techniques that have been considered for diagnosing acute compartment syndrome
include MRI studies, pulse oximetry,62 and sensory testing by vibration exposure.63
INTRAMUSCULAR PRESSURE MEASUREMENT

Abnormally increased intramuscular pressure is the pathogenic mechanism, which
induces the symptoms of acute compartment syndrome. Whenever clinical signs and
60
symptoms are nonconclusive, intramuscular pressure may be measured to conrm

or exclude the syndrome. Measurements of elevated intramuscular pressure are also
helpful to identify patients who do not primarily require surgical treatment, but
initially need nonsurgical treatment. Different methods of intramuscular pressure
measurements are presented and discussed in Chapter 16.
DIRECT NERVE STIMULATION

Painful swollen extremities are commonly seen following trauma. Patients who
are unable to activate their compartment muscles voluntarily may have a nerve
injury, an acute compartment syndrome, painful inhibition of muscle activity, or
any combination thereof. The question arises whether the paralysis is due to a
primary nerve injury or secondary to abnormally increased tissue pressure. Direct
nerve stimulation at the site where the nerve enters the compartment may be a
valuable investigation to estimate the pathogenesis of neuromuscular dysfunction.
A normal response to electrical stimulation of the compartment nerve indicates
that the cause of the paralysis is not a compartment syndrome.64 No muscular
response indicates that the patient has an acute compartment syndrome with no
functioning muscle bers.
IMAGING TECHNIQUES
Imaging technologies such as standard CAT or MRI for diagnosis of acute compartment syndrome are usually not indicated. Treatment should not be delayed to obtain
these studies. They do not add anything essential that cannot be found by the patients
history and by clinical investigation. Imaging techniques may delay diagnosis and
treatment of acute compartment syndrome. An arteriogram is indicated when vascular injury is suspected or repair is indicated.
PULSE OXYMETRY
The pulse oxymeter measures the arterial oxygen saturation of the arterial blood
reaching the compartment, and not the tissue oxygen saturation of the compartment itself. The role of pulse oxymetry in the early detection of acute compartment syndrome has to be determined.62 However, in patients with chronic compartment syndrome, it has been reported to be useful. 65,66 Near-infrared
spectroscopy can detect muscle ischemia, which is caused by acute compartment
syndrome despite severe hypotension and hyperemia, making it potentially useful
in critically injured patients.67
STIMULATION
BY
VIBRATION
Altered perception of vibration stimuli correlated with decreased neutral function

in subjects with elevated intramuscular pressure between 35 and 40 mmHg.63
Alterations in vibratory sensory testing as measured with a 256-cps tuning fork
was found to be an early and reliable indicator of abnormally elevated compartment pressure.
61
TABLE 5.1
Typical Findings of Acute Compartment Syndrome, Arterial Injury, Venous
Occlusion, and Neurapraxiaa
ACS
Arterial
Injury
Increased pressure
Swelling
Erythema
++
++
+
0
0
0
Pain at rest
Pain with stretch
Decreased passive
ROM
Intact pulses
++
++
++
Paresthesia
Paresis
Symptoms
Venous
Occlusion
Neurapraxia
Inflammatory
Reaction
+
+
0
0
0
0
+
+
++
++
+
0
+
+
0
0
0
0
++
+
+
++
++
++
++
++
++
0
0
0
0
++
++
0
0
Stage I
Stage II
Stage III
Note: ACS = acute compartment syndrome; ++ = frequently or always; + = sometimes or to a certain

extent; 0 = seldom or never; ROM = range of motion.
a Symptoms are elicited by the increased intramuscular pressure in Stage I, by the impeded blood
ow in Stage II, and by impaired neuromuscular function in Stage III.
DIFFERENTIAL DIAGNOSIS
It may be difcult to separate symptoms elicited from injury to arteries, veins, and
nerves in patients who are multiply injured. Table 5.1 summarizes some of the
ndings of the different conditions. All the listed ndings of Stage I to Stage III are
positive only in patients with acute compartment syndrome. Patients with arterial
injury have local pain at rest and no arterial pulses distal to the injury. Patients with
venous occlusion have swollen legs, and may have pain at rest and pain with passive
stretch of muscles, e.g., a positive Hohmans sign in the leg. Patients with neurapraxia
have disturbances of sensitivity and motor weakness distally, whereas patients with
inammatory reaction have mild symptoms of compartment syndrome listed in Stage
I and Stage II. Only patients with acute compartment syndrome and neurapraxia
have Stage III symptoms.
SUMMARY
The patients history and ndings at physical examination are the cornerstones in
diagnosing acute compartment syndrome. Development of the syndrome may be
described in three clinical stages that are related to the pathophysiology of the
62
syndrome. In Stage I, patients experience swelling and decreased range of movement

due to increased intramuscular pressure. In Stage II, the pain becomes ischemic due
to impaired muscle blood ow. Passive stretch of affected muscles induces severe
pain. In Stage III, neuromuscular impairment gives motor and sensory dysfunction.
Intramuscular pressure recording and subsequent calculations of local perfusion
pressure are helpful to identify patients with the syndrome.
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64

41. Peck, D., Nicholls, P.J., Beard, C., and Allen, J.R., Are there compartment syndromes
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Acute compartment syndrome of the supraspinatus: a case report, J. Should. Elb.
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44. Cameron, S.E., Acute compartment syndrome of the triceps, Acta Orthop. Scand.,
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45. Holland, D.L., Swenson, W.M., Tudor, R.B., and Borge, D., A compartment syndrome
of the upper arm: a case report, Am. J. Sp. Med., 13, 363, 1985.
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47. Palumbo, R.C. and Abrams, J.S., Compartment syndrome of the upper arm, Orthopaedics, 17, 1144, 1994.
48. Leguit, P., Compartment syndrome of the upper arm, Netherl. J. Surg., 34, 123, 1982.
49. Greene, T.L. and Louis, D.S., Compartment syndrome of the arm a complication
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50. Brumback, R.J., Compartment syndrome complicating avulsion of the origin of the
triceps muscle, J. Bone Jt. Surg., 69-A, 1445, 1987.
51. Gelberman, R.H., Garn, S.R., Hergenroeder, P.T., Mubarak, S.J., and Menon, J.,
Compartment syndromes of the forearm: diagnosis and treatment, Clin. Orthop. Rel.
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52. Gelberman, R.H., Zakaib, G.S., Mubarak, S.J., Hargens, A.R., and Akeson, W.H.,
Decompression of forearm compartment syndromes, Clin. Orthop. Rel. Res., 134,
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53. Peters, C.L. and Scott, S.M., Compartment syndrome in the forearm following fractures of the radial head or neck in children, J. Bone Jt. Surg., 77-A, 1070, 1995.
54. Royle, S.G., The role of tissue pressure recording in forearm fractures in children,
Injury, 23, 549, 1992.
55. Benson, L.S., Sathy, M.J., and Port, R.B., Forearm compartment syndrome due to
automated injection of computed tomography contrast material: case report, J.
Orthop. Trau., 10, 433, 1996.
56. Horlocker, T.T. and Bishop, A.T., Compartment syndrome of the forearm and hand
after brachial artery cannulation, Anesth. Analg., 81, 1092, 1995.
57. Thomas, W.O., Harris, C.N., DAmore, T.F., and Parry, S.W., Bilateral forearm and
hand compartment syndrome following thrombolysis for acute myocardial infarction:
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58. Tompkins, D.G., Exercis myopaty of the extensor carpi ulnaris muscle, J. Bone Jt.
Surg., 59-A, 407, 1977.
59. Oullette, E.A. and Kelly, R., Compartment syndromes of the hand, J. Bone Jt. Surg.,
78-A, 1515, 1996.
60. Salisbury, M.R.E., McKeel, M.D.W., and Mason, A.D., Ischemic necrosis of the
intrinsic muscles of the hand after thermal injuries, J. Bone Jt. Surg., 56-A, 1701,
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61. Spinner, M., Aliache, A., Silver, L., and Barsky, A.J., Impending ischemic contracture
of the hand: early diagnosis and management, Plast. Reconstr. Surg., 50, 341, 1972.
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65
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2051_C06.fm Page 67 Friday, October 10, 2003 8:56 AM
Treatment of Acute
Compartment
Syndromes
INTRODUCTION
The quality of functional results is related to the promptness of treatment. Therefore,

treatment of acute compartment syndrome must not be delayed. The goal of treatment
is to restore a normal neuromuscular function. This is achieved by normalizing the
local perfusion pressure, which is obtained by decreasing the abnormally elevated
intramuscular pressure in the compartment by fasciotomy. Early active treatment to
reduce edema following surgery is important. The wound is closed by secondary
wound closure in most patients with residual swelling after fasciotomy.
GENERAL PRINCIPLES FOR TREATMENT

Early countermeasures to prevent swelling after trauma and to maintain local perfusion pressure are important. Local blood perfusion can be restored in the compartment by the following six steps.
Step 1. Intramuscular pressure decreases by cutting all dressings that give
external compression.
Step 2. Local perfusion pressure in the leg increases when elevation of the
injured limb is concluded.
Step 3. Mean arterial pressure increases by treating hypovolemia.
Step 4. Surgical treatment by acute fasciotomy normalizes intramuscular
pressure.
Step 5. Treatment of postischemic reperfusion prevents crush syndrome from
developing.
Step 6. Postischemic swelling following fasciotomy may be reduced by early
active edema reduction. Each of the steps is discussed in detail.
STEP 1
By cutting all dressings that give external compression, intramuscular pressure
decreases to levels that allow for normal circulation (Figure 6.1).1,2 Elevated intravenous pressure decreases with decreased intramuscular pressure. Intravenous pressure in a compartment can never be lower than intramuscular pressure.3
67
68
Pressure (%)
100
70
35
Cast intact
Cast cut
Cast spread
Webril cut
15
Cast off
Time
FIGURE 6.1 Decrease in intramuscular pressure in a swollen limb by stepwise removal of

plaster cast and bandages. The absolute initial pressure may vary between 60 and 100 mmHg.
STEP 2
Correct treatment by Step 2 requires considering how abnormally increased intramuscular pressure, local intravenous pressure, and mean arterial pressure are affected
by limb elevation. Abnormally elevated intramuscular pressure in a supine subject
does not decrease by elevation of the affected limb.47 Patients tolerance for
increased intramuscular pressure decreases by limb elevation. Local intravenous
pressure in the compartment cannot be decreased by limb elevation, because of
venous congestion. Venous pressure always exceeds local tissue hydrostatic pressure.3 Mean arterial blood pressure decreases by limb elevation.4,8 Therefore, limb
elevation decreases local blood perfusion pressure in patients with impending acute
compartment syndrome (Figure 6.2). Limb elevation is harmful when intramuscular
pressure is abnormally increased and may even, on theoretical grounds, elicit an
iatrogenic acute compartment syndrome.4,8
STEP 3
It is important to maintain the mean arterial pressure by treating the hypovolemia.
The interstitial space is three times larger than the intravascular space in the human
body. Large amounts of uid may rapidly shift from the intravascular space to the
interstitial space in traumatized patients. Fluid shift from the intravascular space into
the interstitial space may cause a predisposition to hypovolemia.
STEP 4
Decompression by fasciotomy is based on typical clinical symptoms and signs. It
normalizes compartment pressure by increasing the compartment size. Residual
Treatment of Acute Compartment Syndromes
69
Limb elevation 35 to 50 cm
FIGURE 6.2 Reduction of local perfusion pressure by 50% if the limb is elevated 35 to 50 cm,
due to decreased mean arterial pressure by 25 to 38 mmHg in the elevated compartment.
muscle tension may be treated by epimysiotomy.9 Techniques for most locations are
discussed later.
STEP 5
Postischemic reperfusion is commonly seen after orthopedic, vascular, or reconstructive
plastic surgery. Limb swelling, muscular dysfunction, or muscle necrosis may complicate treatment by fasciotomy for acute compartment syndrome. Further damage of
muscle tissue may occur on postischemic reperfusion.1012 It is believed that the tissue
damage seen after extended periods of ischemia is a consequence of both ischemia and
reperfusion and not a consequence of the reduced blood ow alone.1013 Oxygen free
radicals may play a critical role in ischemia-reperfusion injury. Free radicals are atoms
or molecules with one or more unpaired electrons, making them extremely reactive and
cytotoxic. Therefore, reoxygenation may induce multifold cellular and vascular permeability alterations. Treatment of ischemic and reperfused tissue with different antioxidants and scavengers may have a salvaging effect in skeletal muscle.14
In an experimental study, bleeding from the muscle following fasciotomy was
no guarantee for tissue viability.15 The results were explained by an abnormal
intramuscular revascularization that distorted the entire intravascular system. The
condition was termed concealed pressure-ischemia contracture. The muscle might
survive partly, but with patchy nonfunctioning areas within it.
STEP 6
Edema reduction should be initiated as soon as possible following fasciotomy. Concentric muscular activity and passive muscular stretch may reduce limb edema. Other
methods include intermittent external compression, limb elevation, and hyperbaric
oxygenation. In uncomplicated cases, wound closure is possible during the third to
fth day after fasciotomy. Methods for edema reduction are discussed in Chapter 18.
70
INDICATIONS FOR SURGICAL TREATMENT

BY FASCIOTOMY
The characteristic symptoms and signs of an acute compartment syndrome are the
best indications for decompression by fasciotomy. However, symptoms and signs
may be difcult to interpret and a denite diagnosis cannot always be made on
clinical grounds alone.16,17 Confusion concerning the indications for decompression
exists. The concept of a critical intramuscular pressure value above which surgical
decompression should be performed is controversial. Some authors advocate the use
of absolute intramuscular pressure values.18,19 Others relate intramuscular pressure
to diastolic blood pressure.20 The authors opinion is that calculations of local blood
perfusion pressure are the best adjunct parameter to a thorough history and clinical
examination. Calculations of perfusion pressure are based on measurements of
intramuscular pressure and mean blood pressure in the arm, as discussed in Chapter
4 on pathophysiology.
Local perfusion pressure below 40 mmHg in traumatized legs impairs muscle
blood ow and impedes normal cellular metabolism.21 Perfusion pressure is the best
parameter to study because it takes into account all the important parameters that
affect tissue nutrition and viability.
TREATMENT BY FASCIOTOMY
Decompression should be done in a bloodless eld whenever possible. The limb
should be kept elevated for 1 or 2 min. No exsanguination method should be used.
The thigh tourniquet should be inated to 100 mmHg above systolic blood pressure.
The surgical procedure seldom takes more than 5 to 10 min to perform during
tourniquet ischemia. Whenever possible, fasciotomy should be done in a bloodless
eld by using a thigh tourniquet. An ipsilateral femur fracture or traumas to the soft
tissues of the thigh are contraindications for the use of a thigh tourniquet. Surgery
performed without a bloodless eld takes much longer time and increases the risks
for iatrogenic tissue damage, especially to the nerves.
The goal of surgical treatment is complete opening of all tight fascial envelopes.
Limited skin incisions or subcutaneous fasciotomy to treat the syndrome must be
avoided for several reasons. Limited exposure may not allow for complete decompression of all the compartments and blind surgical procedures are prone to
iatrogenic tissue damage. The skin envelope contributes to external compression and
a signicantly elevated intramuscular pressure in patients with acute compartment
syndrome.22 The postischemic hyperemia following fasciotomy increases the volume
of the limb further. Limited skin incisions may prevent a normal postoperative limb
swelling caused by dysfunctional endothelial cells.
After fasciotomy is completed, the tourniquet is released. The tourniquet and
the elastic support under the tourniquet, including all bandages on the thigh, are
removed to prevent venous stasis. The viability of the tissues is judged after 5 to 15
min of reperfusion. An initial conservative attitude to muscular excision is recommended. The satellite cells are myogenic cells underneath the basal lamina of the
71
muscle ber. They have a great potential to regenerate muscle tissue.2326 When they
are excised, initially no muscle regeneration occurs.
Delayed treatment of acute compartment syndrome is a clinical challenge. Several authors have reported the results from treatment of patients with high injury
severity score (>30), a delay of more than 35 h to treatment, and an estimated
ischemic time of 56 h.2729 It was recommended that these patients not be treated
surgically until there was a demarcation of a gangrenous part. Even extensive
myonecrosis is not an indication for immediate surgical treatment. Finkelstein and
co-workers concluded that the sequel of infection in a crushed limb after delayed
fasciotomy is much worse than the late muscle contracture that may result from
muscle brosis.27 Sheridan and Matsen reported an infection rate of 46% and an
amputation rate of 21% after late fasciotomy.29
FASCIOTOMY
OF THE
FOOT
Between ve and nine functional compartments have been described in the foot.
Three of the compartments run the entire length of the foot (medial, lateral, and
supercial). Five of them are located in the forefoot (one adductor and four
interossei) and one is located deep in the hindfoot (calcaneal).
There are two approaches to these compartments: the dorsal and the medial. The
dorsal approach to fasciotomy is performed with two longitudinal incisions centered
over the second and fourth metatarsals. The medial incision provides good exposure.
It can be extended proximally to decompress the tarsal tunnel and give access to the
posterior tibial neurovascular bundle. The 5- to 7-cm skin incision starts on the
medial side of the heel, 3 cm from the planta pedis and 4 cm from the back of the
heel. It runs distally parallel to the sole (Figure 6.3). The medial compartment is
opened and the abductor hallucis brevis muscle is reected superiorly. The medial
intermuscular septum is opened longitudinally. Skin closure can usually be performed 5 to 7 days after fasciotomy.
FASCIOTOMY
OF THE
LEG
Several techniques for decompression of leg compartments have been described.30,31

They allow for a complete fasciotomy of all compartments. They must also allow
for a postischemic hyperemia and swelling due to reperfusion.3234 If only the anterior
or lateral compartment is affected without any swelling or tenseness of the posterior
compartments, fasciotomy of the two may be enough. If two or more compartments
are involved in the leg, fasciotomy of all four compartments is recommended. The
recommendation is based on the clinical observation that sometimes the posterior
compartments may swell later than the anterior compartment. By decompressing all
leg compartments, no doubt about remaining acute compartment syndrome exists.
The Parafibular Approach
All compartments of the leg may be decompressed through a single 20- to 30-cm
skin incision over the lateral compartment, 1 cm behind the anterior intermuscular
septum (Figure 6.4).30,35 The supercial peroneal nerve in the peroneus tunnel behind
72
Dorsal incisions
Medial incision
FIGURE 6.3 Fasciotomy of foot compartments. All nine compartments of the foot can be
decompressed through a medial skin incision. By two dorsal incisions centered over the second
and fourth metatarsals, the interosseus compartments are decompressed.
Tibia
Deep posterior
Medial incision
Lateral skin incision

Superficial posterior
Lateral compartment
FIGURE 6.4 All leg compartments may be decompressed by a long, single skin incision
extending from the bular head to the lateral malleolus.
73
Peroneal tunnel
Lateral compartment
FIGURE 6.5 The peroneal nerve often runs in fascial tunnel before it pierces the fascia about
10 to 12 cm proximal of the lateral malleolus.
the anterior intermuscular septum 10 to 12 cm proximal of the lateral malleolus is

identied and protected. If the nerve passes through a peroneal fascial tunnel, it may
be decompressed by opening the tunnel all the way until it enters into the muscle
belly proximally.36 The lateral compartment is opened 1 cm behind the anterior
intermuscular septum (Figure 6.5). The fascia over the anterior compartment is
exposed by subcutaneous dissection toward the anterior ridge of the tibia. It is divided
longitudinally over the proximal muscle bellies and distally all the way to the
retinaculum. The line of fascial incision follows 1 or 2 cm lateral of the anterior
margin of the tibia. The deep posterior compartment is opened from behind the
bula by following the posterior intermuscular septum and releasing the soleus
muscle attachment from the proximal third of the bula.
Double-Incision Fasciotomy
Double-incision fasciotomy has been advocated by Mubarak et al.31 It is performed
through a lateral and a medial skin incision. The lateral incision is identical to the
parabular approach described previously.
The supercial and deep posterior compartments are opened by a 20- to 30cm-long skin incision 4 cm behind the posterior margin of the tibia. By this skin
incision, damage to the branches of the saphenous nerves and veins is avoided to
some extent. By dissecting close to the fascia toward the posteromedial margin of
the tibia, the nerves and veins may be reected anteriorly. One half of the skin on
the anterior circumference of the leg should be left, and the second half of it on the
posterior side. The fascia covering the soleus and gastrocnemius muscle bellies is
opened. More distally and about 1 cm from the posterior margin of the tibia, the
fascia over the exor digitorum longus muscle is divided. If the soleus muscle has
74
a very distal attachment to the tibia, it is often necessary to detach the muscle between
3 cm and up to 8 cm from the tibia in a proximal direction to allow for full
decompression of the muscles in the deep posterior compartment, including the
posterior tibialis muscle. Others have suggested limited skin incisions of 15 cm31
and even subcutaneous fasciotomy.37 However, skin as a limiting factor for decompression in patients with acute compartment syndrome has been reported.22 Therefore, limited skin incisions should be avoided. Furthermore, subcutaneous fasciotomies of the posterior compartment are too traumatic to the muscles, nerves, and
veins. This author strongly discourages blind surgery through small skin incisions
in this location.
If the patient has a contusion or other severe trauma to the pretibial soft tissues,
surgery by double incision may create an anterior distally based cutaneous lambeau.
This may lead to increased risk for skin and soft tissue necrosis and wound-healing
problems. Therefore, this author prefers the lateral, single parabular approach in
such cases. Double-incision fasciotomy may be used in cases when surgery in
bloodless eld is not possible, e.g., in patents with ipsilateral femur fractures. It is
a good alternative for surgeons who are not familiar with the single, lateral incision
technique, which is also technically more demanding.
Transinterosseous Decompression
Through a similar skin incision as described for the parabular fasciotomy, the lateral
compartment is opened behind the anterior intermuscular septum. The supercial
peroneal nerve and the peroneus longus muscle are reected anteriorly. The posterior
supercial compartment is opened by splitting the posterior intermuscular septum.
The anterior compartment is opened anterior to the anterior intermuscular septum.
By reecting the extensor digitorum longus muscle and the anterior tibial neurovascular bundle forward and medially toward the tibia, the interosseous membrane is
exposed. Over the tip of a right-angled clamp a puncture of the interosseous membrane is extended distally close to the bula.38
Disadvantages of this technique include bulging of swollen muscles from the
deep posterior compartment through the fascial incision. Shear forces at the foramen
of the interosseous membrane may compress the vessels. This may induce a venous
stasis of the anterior compartment because the vasculature is an end artery system.
Furthermore, the interosseous membrane is a part of the stability of the proximal
and distal syndesmosis between the tibia and the bula.
In most cases of trauma, a four-compartment fasciotomy is necessary. If
the syndrome develops in one compartment, other compartments are prone to
reactive swelling. The symptoms of an impending syndrome may also be delayed
in other compartments.
Fibulectomy
Decompression by bulectomy3942 is not recommended because of its inferior results
and increased risks for disability. During this procedure, the peroneal vessels and
their paired venae comitantes may be damaged.38
75
FIGURE 6.6 Intraoperative photo of the lateral thigh. The skin incision should be complete
from the greater trochanter to the lateral femoral condyle. (See color insert following page 106.)
FASCIOTOMY
OF THE
THIGH
There are three compartments of the thigh: anterior, posterior, and medial. The psoas
muscle may be considered as a separate compartment.43 Patients with compartment
syndrome of the thigh are decompressed by a lateral approach (Figure 6.6).44 The
anterior and posterior compartments are decompressed by incision of the fascia lata
and the lateral intermuscular septum after retraction of the vastus lateralis muscle
(Figure 6.7). The technique has been used by several authors.4549
FASCIOTOMY
OF THE
GLUTEAL COMPARTMENTS
The gluteal compartment syndrome is uncommon. It must be considered as a potential complication of trauma to the pelvic ring. A conservative approach has been
advocated. Five out of six patients with swelling of the gluteal muscle compartments,
rhabdomyolysis, myoglobinuria, and sciatic nerve palsy of the contralateral leg were
treated conservatively. Symptoms resolved in all of them.50 Isolated gluteal compartment syndrome does not increase the risk for crush syndrome.51 If the patient
has clinical signs of simultaneous active bleeding, arteriography of the pelvis may
be performed before a fasciotomy.52
Skin incision to decompress the gluteal compartments may be a curved incision
parallel to the iliac crest or a posterior curved incision from the posterior iliac spine
to the greater trochanter.53 A third alternative is exposure with a double curved
incision that runs from the posterior iliac spine over the greater trochanter down to
the level of inferior gluteal fold. The incision is then brought medially beneath the
buttocks and down to the midposterior thigh (Figure 6.8).54 The tensor fascia lata is
opened by fasciotomy.51,55 The gluteus maximus muscle is decompressed by multiple
epimysiotomies.56 The gluteus medius is decompressed by epimysiotomy.51 In
patients with sciatic or peroneal nerve palsy, the sciatic nerve must be inspected
intraoperatively to exclude direct damage to the nerve.
76
Medial incision
Lateral incision
FIGURE 6.7 The three thigh compartments may be decompressed through a single, straight
lateral skin incision or through an additional medial skin incision.
FIGURE 6.8 Gluteal compartments can be decompressed by a curved incision parallel to the
iliac crest to the greater trochanter. The gluteal muscles may need multiple fasciotomies and
epimysiotomies because they are multipennated.
FASCIOTOMY
OF THE
77
DORSOLUMBAR COMPARTMENT
Fasciotomy may be done through separate skin incisions between 2 and 4 cm lateral
to the spinous processes. A midline skin incision may also be used.57
FASCIOTOMY
OF
SHOULDER MUSCLES
The shoulder includes several compartments. The supraspinatus, infraspinatus, and

subscapularis muscles are enclosed in osteofascial compartments, whereas the trapezius and deltoid muscles have more compliant locations. The possibility of a compartment syndrome of the shoulder has been suggested.58 However, there are few reports
of the syndrome in this location.5860 The supraspinatus muscle generates high intramuscular pressure during contraction.61 However, this is not a sign of volume load of
the muscle, but rather a sign of its muscular architecture and force generation.62
FASCIOTOMY
OF THE
UPPER ARM
The upper arm has two compartments: the extensor compartment enclosing the triceps
muscle and the exor compartment enclosing the biceps muscle bellies. The compartment is less rigid than other leg and arm compartments. A longitudinal incision on the
medial aspect of the arm from the shoulder to the elbow over the medial intermuscular
septum will allow for decompression of both the biceps and triceps compartments
(Figure 6.9). Delayed primary closure may be performed after 4 or 5 days.63
FIGURE 6.9 The anterior and posterior compartments of the upper arm can be reached by
a skin incision over the medial neurovascular bundle.
78
FASCIOTOMY
OF THE
FOREARM
Four compartments of the forearm have been described: the supercial and deep
volar, the dorsal, and the extensor indicis proprius muscle, which is located in a
different fascial envelope and may need a separate fasciotomy. Surgery should be
done in a bloodless eld whenever possible.
Fasciotomy of the Volar Compartments
The volar incision according to Gelberman64 originates 2 cm proximal to the
medial epicondyle. It is extended obliquely across the antecubital fossa and
further distally to reach the volar aspect of the forearm. The incision is extended
ulnar to the palmaris longus tendon to avoid injury to the cutaneous branch of
the median nerve. It crosses the wrist crease at an angle to avoid exposure and
transmission of tensile forces during wound healing. The incision is extended
into the midpalm (Figure 6.10). A curvilinear skin incision has also been
described. Finally, the volar aspect of the forearm can be decompressed by a
straight volar incision on the ulnar side, which starts proximal to the elbow and
radial to the biceps tendon.64 The supercial exors are decompressed by a
complete fasciotomy (Figure 6.11A). The deep exors are exposed by retracting
the supercial exors (Figure 6.11B). The tourniquet used for a bloodless eld
is removed and muscles are mobilized, inspected, and judged for viability signs.
Individual muscles may need epimysiotomy. Liqueed muscles should be
removed at this time. The median nerve in the carpal tunnel is decompressed to
avoid an edge effect on the nerve at its proximal entrance in the tunnel. The
median nerve may also need proximal decompression at the lacertus brosis and
at the pronator teres muscle as well.65 The ulnar nerve is decompressed when
indicated by clinical signs by opening the Guyons tunnel.
FIGURE 6.10 Suggested skin incisions to decompress the compartments of the forearm and
the interossei muscles of the hand. The carpal tunnel must be decompressed in all cases of
acute compartment syndrome of the forearm.
79
A.
B.
C.
FIGURE 6.11 Decompression of the volar compartments of the forearm and secondary suture
of the wound. (A) The carpal tunnel and the supercial exors are decompressed. (B) By
retracting the supercial exors, the deep compartment is decompressed. (C) The skin over
the carpal tunnel should be sutured primarily whenever possible.
Fasciotomy of the Dorsal Compartment

A straight longitudinal incision is carried from 5 cm distal to the lateral epicondyle
and extended about 10 cm distally. The fascia covering M. extensor indicis proprius
may need a separate fasciotomy.
FASCIOTOMY
OF THE
HAND
The hand includes six to ten compartments. The ten compartments include the
hypothenar, thenar, adductor pollicis compartments, the four dorsal interossei compartments, and the three volar interossei compartments. All compartments with
abnormally increased intramuscular pressure must be treated. Besides, most patients
with acute compartment syndrome of the hand must have a carpal tunnel decompression and sometimes also decompression of the ulnar nerve.66 The dorsal
interossei muscles may all be reached through two dorsal skin incisions, one over
the second metacarpal bone and another over the fourth metacarpal bone (Figure
6.10). It is important to decompress the carpal tunnel and Guyons tunnel in all cases
of sensory dysfunction.
80
POSTOPERATIVE MANAGEMENT
EDEMA REDUCTION
Intensive edema-reducing therapy is important following surgery by fasciotomy.
Edema-reducing methods are outlined in Chapter 18. They include active muscle
contractions, passive muscle stretch, intermittent external compression, limb elevation, and hyperbaric oxygenation.
Following decompression, the limb is immobilized. Early active exercises to
reduce edema formation are important. Following successful edema reduction, the
wound may be closed by secondary closure after 3 to 4 days in many patients.35,67
Patients with acute compartment syndrome of the leg and soft tissue trauma to the
ipsilateral thigh are more difcult to treat. These patients may need repeated wound
adaptation 5 to 7 days after trauma. Secondary wound closure is also more difcult
in patients with diabetes and in those who cannot walk or activate their limb muscles
for other reasons. Continuous epidural anesthesia should therefore be used cautiously. This authors experience is that this treatment of pain induces muscular
dysfunction that impairs edema reduction. Alternative pain treatment should be
considered in these patients if muscular activity cannot be maintained. Edema
reduction by concentric muscular activity is a prerequisite for successful early
secondary wound closure.
SECONDARY WOUND CLOSURE
BY
DERMATOTRACTION
Creep occurs when skin is stretched under a constant force. The skin will continue to
extend if the force is kept constant. Stress relaxation occurs when the skin is stretched
for a given distance, which is held constant. Several techniques are available to facilitate
the closure of wounds following fasciotomy for acute compartment syndromes, such as
(1) progressive closure by wire sutures or tape, (2) ETE tension bands,67,68 (3) dermatotraction by Sure-Closure,69 (4) a rod-tensioning device,70 or (5) Kirschner wires.71
Secondary Closure by Wire Sutures
Secondary wound closure by wire sutures may be done on the third or fourth day
following surgery if treatment by edema reduction has been successful.35 Placement
of static tensioning devices across the wound includes tape30 or sutures,35 which are
replaced or tightened. Intramuscular pressure must not exceed 30 to 35 mmHg at
secondary wound closure.35 Treatment in this way makes skin transplantation unnecessary. The results of secondary wound closure are cosmetically more appealing
than skin transplantation (Figure 6.12). The wound heals quicker and the time for
in-hospital stay is shorter.
Silicon or Rubber Bands
Elastic tensioning devices have the advantage of providing continuous pull on wound
edges. They may be tightened without replacement and without the need for anesthesia.72 Tightening is performed by pulling each segment of the vessel loop. The
81
(A)
(B)
(C)
FIGURE 6.12 Secondary wound closure by wire sutures in a patient 3 days after fasciotomy
for acute compartment syndrome of the thigh. (A) The lateral thigh wound 3 days after
fasciotomy. (B) Wire sutures are applied 3 days after fasciotomy. (C) On Day 5, the sutures
are tightened to completely close the wound. (See color insert following page 106.)
excess of the loop may be tied to the last staple. By using an elastic vessel loop
shoelace, delayed primary closure is achieved within 9 days.
External Tissue Extender (ETE)
Each ETE unit consists of a silicon band connected to two friction stoppers. The units
may be connected to each other by hinges (Figure 6.13). The silicon bands can be
tightened twice daily without anesthesia. In this way, the wound edges are approached.
When the wound gap is between 10 and 15 mm, it can be closed by ordinary sutures.
The ETE technique is a valuable tool in patients who have difculties in reducing their
82
FIGURE 6.13 Dermatotraction by external tissue extender (ETE) in a patient treated by

parabular fasciotomy due to acute leg compartment syndrome. Treatment by external tissue
extender was initiated on Day 3 after decompression.
limb edema. The ETE device decreases limb volume by increasing the interstitial
hydrostatic pressure to levels that do not impair local perfusion pressure.35,67
Sure-Closure
The device consists of two 7.5-cm-long pins, each of which is threaded through the
dermis on either side of the wound. Two U-shaped arms are hooked to the pins
(Figure 6.14). The distance between the wound edges is decreased and a threaded
screw that passes through the arm increases the tension. By using a tension of 3 N
or less, intramuscular pressure in the leg remains under 30 to 35 mmHg.73
Other Methods of Dermatotraction
A simple method using 2-mm Kirschner wires through the skin has been described
(Figure 6.15).71 The skin edges can also be approached by another technique that
A.
B.
FIGURE 6.14 (A) Schematic illustration of secondary wound closure by Sure-Closure. (B)
The tensile forces acting over the wound edges can be kept constant at a desirable level by
a threaded screw.
83
(A)
(B)
FIGURE 6.15 (A) Subcutaneously inserted Kirschner wires, which are caught by a wire
suture at the crossing point. (B) At this time the skin edges are approached. The sound may
be closed by ordinary stitches.
includes a rod-tensioning device combined with a transparent polyurethane adhesive

sheet that sticks rmly to the skin and to the rod, but not to the moist wound. Each
day the rod must be lifted and turned one complete turn and then laid back in the
rack, which prevents unrolling.70
Wounds that are treated by delayed closure are as strong as primary closed
wounds. This means that an ischemic wound can safely be left open for 3 days
before suturing without affecting the biomechanical properties.74
VACUUM-ASSISTED WOUND CLOSURE

The wound is exposed to subatmospheric pressure of about 125 (50 to 200) mmHg.
A sterile polyurethane sponge is cut to t with the entire wound surface. An adherent
plastic sheet is placed to cover the wound and the tubing, which is connected to a
reservoir and a pump. Edema uid is removed from the extravascular space. The
84
mechanical tension stimulates proliferation of granulation tissue. Following fasciotomy, a higher proportion of vacuum-treated wounds undergo primary closure, making skin grafting unnecessary.
SKIN GRAFTING
Skin grafting gives poor coverage and sensation to the wound, and it is less appealing
cosmetically. In most cases, skin grafting can be avoided following fasciotomy for
acute compartment syndrome. The key point is to reduce the posttraumatic limb
edema early after fasciotomy.
ROLE
OF
HYPERBARIC OXYGENATION
Hyperbaric oxygen therapy provides hyperoxygenation of the tissues. Oxygen

dissolves in plasma in direct proportion to its partial pressure. Treatment by
hyperbaric oxygenation is therefore a supplement of the oxygen-carrying capacity of red blood cells. Tissues can remain viable without hemoglobin-borne
oxygen if the patient breathes pure oxygen at 2.4 atm absolute pressure. Treatment by oxygen induces mild vasoconstriction and simultaneously elevates
partial pressure of oxygen levels. Vasoconstriction lowers capillary pressure,
altering the Starling equilibrium in a way that promotes absorption of interstitial
edema. Injury induced by ischemia-reperfusion can be reduced by hyperbaric
oxygenation treatment.
Hyperbaric oxygen therapy has been used as an adjunctive treatment in patients
with ischemic injury following trauma. The high oxygen tension in arterial blood
achieved with hyperbaric oxygen therapy increases the wound oxygen tension in
previously hypoxic wounds.75 Hyperbaric oxygenation restores oxygen tension to
normal and enhances healing. It reduces postischemic edema76 and skeletal muscle
necrosis in skeletal muscle injury77 and in acute compartment syndrome.78,79 It has
been suggested that treatment by hyperbaric oxygenation can arrest the progression
of abnormally increased intramuscular pressure during the lag phase in acute compartment syndrome.
When tissue oxygenation levels decrease, the ability of leukocytes to handle
infection is markedly reduced. A tissue oxygen tension of 30 mmHg (4 kPa) is
required for broblast function during wound healing. Thus, treatment by hyperbaric
oxygenation may maintain tissue viability during an initial hypoxic phase, prevent
infection, promote healing, and restore function of the injured tissues. It improves
metabolic restitution in postischemic skeletal muscle.80
Hyperbaric oxygenation treatment enhances the recovery of blood ow and
functional capillary density in postischemic tibialis anterior muscle.81 It improves
wound healing. Hyperbaric oxygenation is recommended as a useful adjunct in
management of severe (Grade III) crush injuries of the limbs in patients over
40 years of age.82 Hyperbaric oxygenation can be used in patients with obvious
necrosis at the time of decompression, when massive edema exists and in patients
who have impaired ability to reduce edema by other means, e.g., patients with
neuropathy.
85
SUMMARY
The goal of treatment of acute compartment syndrome is to restore normal neuromuscular function. This is achieved by normalizing the local perfusion pressure,
which is obtained by decreasing the abnormally elevated intramuscular pressure.
The following six easy steps may treat the syndrome. Local perfusion pressure in
the compartment can be restored by (1) cutting all dressings that give external
compression, (2) concluding limb elevation, (3) increasing mean arterial pressure
by treating hypovolemia, and (4) normalizing intramuscular pressure by fasciotomy.
Whenever possible, fasciotomy should be performed in a bloodless eld. The tourniquet should be removed from the limb immediately after pressure is deated. (5)
The fth step includes treatment of postischemic reperfusion and the crush syndrome
that may follow fasciotomy by early active edema reduction. (6) The sixth step is
prescribing treatment for edema reduction. Concentric muscular activity is one of
the most powerful edema-reducing mechanisms. This should be taught to the patient.
Following successful edema reduction, the wound may be closed 3 to 5 days after
fasciotomy in most cases. In some cases, closure by dermatotraction is very helpful.
Skin grafting can be avoided in most patients. Hyperbaric oxygenation is recommended as a useful adjunct in management of severe crush injuries, especially in
patients over 40 years of age.
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78-A, 1515, 1996.
67. Wiger, P., Blomquist, G., and Styf, J.R., Wound closure by dermatotraction after
fasciotomy for acute compartment syndrome, Scand. J. Plast. Reconstr. Surg. Hand
Surg., 34, 315, 2000.
68. Blomqvist, G. and Steenfors, H., A new partly external device for extension of the
skin before excision of skin defects, Scand. J. Plast. Reconstr. Hand Surg., 27, 179,
1993.
69. Hirshowitz, B., Lindenbaum, E., and Har-Shai, Y., A skin-stretching device for the
harnessing of the viscoelastic properties of skin, Plast. Reconstr. Surg., 92, 260, 1993.
70. Bulstrode, C.J.K., King, J.B., Worpole, R., and Ham, R.J., A simple method for
closing fasciotomies, Ann. Roy. Coll. Surg., 67, 119, 1985.
71. Bashir, A.H., Wound closure by skin traction: an application of tissue expansion, Br.
J. Plast. Surg., 40, 582, 1987.
72. Harris, I., Gradual closure of fasciotomy wounds using a vessel loop shoelace, Injury,
24, 565, 1993.
73. Styf, J., Karladani, A., and Wiger, P., Secondary wound closure, unpublished.
74. Quirinia, A. and Viidik, A., Effect of delayed primary closure on the healing of
ischemic wounds, J. Trau., 41, 1018, 1996.
89
75. Shefeld, P.J., Tissue oxygen measurements with respect to soft-tissue wound healing
with normobaric and hyperbaric oxygen, HBO Rev., 6, 18, 1985.
76. Nylander, G., Lewis, D., Nordstrm, H., and Larsson, J., Reduction of postischemic
edema with hyperbaric oxygen., Plast. Reconstr. Surg., 76, 596, 1985.
77. Haapaniemi, T. and Nylander, G., Hyperbaric oxygenation reduces ischemia-induced
skeletal muscle injury, Plast. Reconstr. Surg., 97, 602, 1996.
78. Strauss, M.B., Hargens, A.R., Gershuni, D.H., Greenberg, D.A., Crenshaw, A.G.,
Hart, G.B. et al., Reduction of skeletal muscle necrosis using intermittent hyperbaric
oxygen in a model compartment syndrome, J. Bone Jt. Surg., 65-A, 656, 1983.
79. Skyhar, M.J., Hargens, A.R., Strauss, M.B., Gershuni, D.H., Hart, G.B., and Akeson,
W.H., Hyperbaric oxygen reduces edema and necrosis of skeletal muscle in compartment syndromes associated with hemorrhagic hypotension, J. Bone Jt. Surg., 68-A,
1218, 1986.
80. Haapaniemi, T., Hyperbaric oxygenation treatment attenuates glutathione depletion
and improves metabolic restitution in postischemic skeletal muscle, Free Rad. Res.,
23, 91, 1995.
81. Sirsjo, A., Lehr, H.A., Nolte, D., Haapaniemi, T., and Lewis, D.H., Hyperbaric oxygenation treatment enhances the recovery of blood ow and functional capillary
density in postischemic striated muscle, Circ. Shock, 40, 9, 1993.
82. Bouachour, G., Cronier, P., and Gouella, J.P., Hyperbaric oxygen therapy in the
management of crush injuries: a randomized double-blinded placebo-controlled clinical trial, J. Trau., 41, 333, 1996.
Acute Abdominal
INTRODUCTION
Today more patients survive the initial phase of high-energy multitrauma that once
was fatal. Therefore, patients with multifactorial organ dysfunction, including
patients with abnormally elevated intraperitoneal hydrostatic pressure, are more
likely seen. Abnormally elevated intraabdominal pressure may cause acute abdominal compartment syndrome. Diagnosis and treatment of the syndrome are difficult
because patients have multiple injuries and present a complex clinical picture. The
elevated intraabdominal pressure induces respiratory, cardiovascular, renal, and visceral dysfunction. It even affects the central nervous system in humans.1,2 Acute
abdominal compartment syndrome is lethal if left untreated.
Elevated intraabdominal pressure, increased intraperitoneal hydrostatic pressure, and intraabdominal hypertension have been used synonymously. They
represent clinical conditions that are initially benign and reversible. When
intraabdominal pressure is abnormally elevated or intraabdominal hypertension
acts during an extended period of time, the condition may evolve to an acute
abdominal compartment syndrome. The syndrome is irreversible and requires
surgical treatment by decompression. The mortality rate among patients with
acute abdominal compartment syndrome is up to 60%.3 In a review, Schein and
co-workers reported on 45 patients with acute abdominal compartment syndrome; 19 of these (42%) died.4
DEFINITION
Acute abdominal compartment syndrome is defined as increased intraperitoneal
hydrostatic pressure to levels that impair local blood perfusion pressure and induce
dysfunction of the intra- and retroperitoneal organs. The elevated intraabdominal
pressure induces respiratory, cardiovascular, and renal dysfunction. Acute abdominal
compartment syndrome is the end result of a progressive elevation of intraabdominal
pressure that leads to multiple organ dysfunction.
Intraabdominal hypertension has been defined as intraabdominal pressure
exceeding 15 to 18 mmHg ( = 20 to 25 cm H2O).5 It is a preliminary stage that,
when left untreated, may lead to a clinically manifest acute abdominal compartment
syndrome. Intraabdominal hypertension can be considered an early indication of
acute abdominal compartment syndrome.
91
92
INCIDENCE
The incidence of acute abdominal compartment syndrome varies with clinical setting
and definition of the syndrome. In a study, the syndrome was diagnosed in 21 of
145 patients (14%) with abdominal trauma and with injury severity score exceeding
15 points.6 In this study, 60% of patients had blunt trauma and 67% required
abdominal packing during the initial operation. In other studies, the incidence of the
syndrome is reported to be 4% in patients with repair of aortic rupture7 and 15% in
patients who required laparotomy and packing.3
HISTORICAL PERSPECTIVES
The associations between increased intraabdominal pressure and dysfunction of
different abdominal and thoracic organs have been known for more than 100 years.
Weber in 1851 and Donders in 1854 suggested that physiological oscillations of
intrathoracic and intraabdominal pressures during respiration assisted venous return
from the abdominal to the thoracic cavity.8 Later, Marey in 1863 and Bert in 1870
demonstrated the association between respiration and intraabdominal pressure.9,10 In
1878, Quincke showed that abdominal pressure in patients with ascites exceeded
atmospheric pressure.8 He also described that increased abdominal pressure impaired
venous return from the viscera. Emmerson concluded that distension of the abdomen
by fluid or gas raises abdominal pressure.8
In 1890, Heinricus described pulmonary dysfunction secondary to increased
intraabdominal pressure in an experimental study, and in 1900 Schaefer pointed out
that the tone of the abdominal wall muscles is regulated by the respiratory center.8,11
Intraabdominal pressure exceeding 20 to 33 mmHg killed small animals by fatiguing
the diaphragm and diminishing venous return to the heart.8
The effects of increased intraabdominal pressure on renal function were first
described by Wendt in 1873 and later by Bradley and Bradley in 1947.12,13 They
reported that increased intraabdominal pressure induced oliguria. It has been shown
in experimental studies that constant distension of the abdomen by inflating a
balloon, which had been surgically inserted into the abdomen, caused death.14 Renal
decapsulation was first performed by Harrison in 1896.15
In the 1940s, mortality rates following treatment of large omphaloceles by
forceful closure of the abdominal wall was reported. The abdominal crowding
induced respiratory failure and cardiovascular collapse. Later, in the 1960s and
1970s, physicians became more aware of the potentially hazardous effects of
increased intraabdominal pressure during laparoscopy.16 The term acute abdominal
compartment syndrome was first used by Kron et al. in 1984.17 Currently, the
syndrome refers to the consequences of abnormally elevated intraabdominal pressure
regardless of cause.
ETIOLOGY AND PATHOGENESIS

Acute abdominal compartment syndrome may follow posttraumatic hemorrhage and
abdominal surgery. The mechanisms that induce acute abdominal compartment
Acute Abdominal Compartment Syndrome
93
syndrome are usually multiple and the pathogenetical factors are additive.18,19 The
syndrome has also been documented in patients with tense ascites, necrotizing
pancreatitis, megacolon, and retroperitoneal hematoma.7,20,21 Three different mechanisms may increase intraabdominal pressure to abnormal levels: (1) increased intraor retroperitoneal volume, (2) external compression, and (3) decreased size of the
abdominal compartment.
INCREASED INTRAABDOMINAL VOLUME

Hemorrhage, edema, bowel distension, obstruction of mesenteric veins, tense ascites,
and abdominal packs, as well as peritonitis and tumor cause increased intraabdominal
volume.3,2226 Severe bowel edema may follow prolonged ischemia, e.g., following
surgery on the abdominal aorta.7,27,28 Laparoscopy with CO2 pneumoperitoneum has
been shown to have adverse effects on cardiovascular and renal function in
experimental29 and clinical studies.3032 Acute abdominal compartment syndrome
can occur with no abdominal injury in patients with severe hypovolemic shock33
and in patients with coagulopathy.28
External compression of the abdomen increases intraabdominal pressure. This may
be caused by pneumatic antishock garments34,35 and by tight abdominal closures.3,22,26
External compression by military antishock trousers may also increase intraabdominal pressure.3638
DECREASED COMPARTMENT SIZE

Repair of abdominal wall defects or large incision hernias may increase intraabdominal
pressure by decreasing the compartment size. Decreased abdominal volume may be
due to loss of the abdominal wall and to increased tension of the abdominal wall
muscles. Increased intrathoracic pressure may also depress the diaphragm and thereby
decrease the abdominal volume, which results in increased intraabdominal pressure.
Elevated intraabdominal pressure is seen in patients with burn injuries with
abdominal eschars.34,35 Acute abdominal compartment syndrome was reported in
two patients with more than 70% of the body surface burned.39 Patients with circumferential torso burns are at increased risk for the syndrome.
PATHOPHYSIOLOGY
Hydrostatic pressure in the peritoneal cavity interacts with pressure in the thoracic
cavity, retroperitoneal space, and lower extremities. Understanding the mechanical
and physiological interaction between increased intraperitoneal pressure and other
body compartments is helpful in the clinical diagnosis of patients with severe
abdominal injury (Figure 7.1).
Intraabdominal pressure exceeding 10 to 25 mmHg decreases cardiac output,
induces respiratory dysfunction, and declines renal function. Multiorgan system
failure evolves if the pressure is not promptly relieved.18 Abnormally elevated
94
A.
C.
D.
E.
B.
Venous pressure
Lower extremity
Intraperitoneal space Intrathoracic space Intracranial space
FIGURE 7.1 The intraperitoneal compartment (A), the intrathoracic compartment (B), the
intracranial compartment (C), the extremity compartments, (D) and the retroperitoneal compartments (E). The figure illustrates how elevated intraabdominal pressure is transmitted to
the other compartments by pushing the diaphragm upward. The elevated intraperitoneal
venous pressure is also transmitted by the waterfall mechanism (pooling of blood) to all the
other body compartments. Patients with abnormally elevated intraperitoneal hydrostatic pressure have pulmonary and cardiovascular dysfunction. Intracranial and extremity pressures
increase due to venous stasis.
intraabdominal pressure impairs renal blood flow, pulmonary function, and cardiac
function. It may cause bowel ischemia and affect intracranial pressure.
Increased intraabdominal pressure reduces abdominal wall blood flow, which
leads to ischemia and edema.40 Both the venous return and cardiac output fall as
intraabdominal pressure rises as little as 10 mmHg.41 The effects of increased
intraabdominal pressure on respiratory and cardiovascular, renal, visceral, and neurologic function are discussed next.
RESPIRATORY FUNCTION
Elevated intraabdominal pressure pushes the diaphragm upward (Figure 7.1). The
total lung capacity and functional residual capacity decrease by 40% when intraabdominal pressure increases from about 2 to 12 mmHg.42 This may lead to compression of the lung tissue and atelectasis, which in turn may create a shunt of unoxygenated blood.18,41,42 The volume and compliance of the thoracic cavity decrease.
The end inspiratory pressure increases. The dynamic and static compliances of lung
tissue decrease. Tissue oxygenation decreases and carbon dioxide increases.43 The
pulmonary end expiratory pressure required to deliver a fixed tidal volume increases
significantly by intraabdominal pressure above 25 mmHg. Pulmonary wedge pressure increases with increasing intraabdominal pressure.44 It has been suggested that
the high pulmonary elastance seen in experiments of increased intraabdominal pressure is due to decreased chest wall compliance associated with decreased intrathoracic volume because of the elevated diaphragm.7 Peak inspiratory pressure is high
during mechanical ventilatory support.18 Increased intraabdominal pressure is a
major determinant of respiratory dysfunction in diaphragmatic rupture.45
95
CARDIOVASCULAR FUNCTION
Cardiac Function
Intraabdominal pressure of 10 to 15 mmHg decreases cardiac output significantly.41
By 20 mmHg, cardiac output decreases by 15% in normovolemic dogs and by 50%
in hemorrhaged dogs.46 The elevated intrathoracic pressure impairs the stroke volume, decreases venous return, and decreases cardiac filling pressure as well as
increases vascular resistance of the systemic circulation.41,47,48 Intraabdominal pressure of 40 mmHg produced by inflation of a pneumatic antishock garment decreases
cardiac output.45 In summary, cardiac depression is related to increased peripheral
resistance46 and diminished venous return,41 or both.
Arterial Pressure
The mean arterial pressure of the lower extremities is not affected by elevated
intraabdominal pressure. In an experimental study, the mean arterial pressure did
not change significantly when intraabdominal pressure was elevated to 20 mmHg
during pneumoperitoneum.49 Little difference between brachial and femoral arterial
pressure was observed when intraabdominal pressure was increased up to 70
mmHg.50 This indicates that mean arterial pressure in the lower limbs is not decreased
by abnormally elevated intraabdominal pressure.
Venous Return
Increased intraabdominal pressure is transformed to all intraabdominal and retroperitoneal veins. Increased intraabdominal pressure is also transformed into the
retroperitoneal space (Figure 7.1). About 90% of the increased intraabdominal pressure is reflected in femoral venous pressure.50,51 This means that changes of inferior
vena cava pressure parallel intraabdominal pressure. Venous return depends on the
resistance of the veins and on the upstream driving pressure for venous return. It
has been shown to be impaired at an intraabdominal pressure of 15 mmHg46 and
30 mmHg.52 Rubinson and co-workers showed with angiographic observations in
experimental studies that the inferior vena cava was obstructed at the diaphragm
when the hydrostatic pressure difference was 28 mmHg.52 Venous pressure in the
limbs increases to levels above intraabdominal venous pressure.
In normovolemic patients, cardiac output usually does not fall significantly until
intraabdominal pressure is 40 mmHg.53 This pressure level increases pressure in the
vena cava inferior and venous return from the lower extremities decreases.54 The
mechanism for this is the waterfall phenomenon (Figure 7.1).55,56 In hypovolemic
conditions, even lower abdominal pressures can be harmful because both the inferior
vena cava and the arterioles are collapsed at lower pressures.
Perfusion Pressure
Elevated intraabdominal pressure decreases perfusion pressure of the intraabdominal
organs. Elevated tissue hydrostatic pressure and venous pressure are the causes for
the decreased perfusion pressure.
96
RENAL FUNCTION
Postoperative anuria or oliguria in a patient after closure of a tensely distended
abdomen may be caused by abnormally elevated intraabdominal pressure. Intraabdominal pressure of 20 mmHg impairs renal function by reducing glomerular filtration rate and renal blood flow.47 Intraabdominal pressure of 30 to 40 mmHg may
induce anuria.18,27,29,47,57 Renal vascular resistance increases over 500% when intraabdominal pressure is elevated from 0 to 20 mmHg.18,57 The dysfunction is reversible.
It has been reported that 80% of the inflated pressure of the antigravity suit is
transmitted to the retroperitoneal space.36 Harman et al. showed that impaired renal
function was not due to urethral compression.47 They observed no significant difference in any parameters of hemodynamic or renal function in dogs with and without
urethral stents. Therefore, urethral compression was excluded as a cause of renal
dysfunction. One reason for this may be that the renal collecting system can generate
hydrostatic pressures up to 90 mmHg. It has been suggested that direct compression
of the kidneys by increased intraabdominal pressure may elevate cortical pressure,
leading to an acute renal compartment syndrome.20 Sugrue and co-workers found
an association between increased intraabdominal pressure and renal impairment in
patients admitted to an intensive care unit after laparoscopy.58
VISCERAL ABNORMALITIES
The gut is the most sensitive organ to elevated intraabdominal pressure. Elevated
intraabdominal pressure may reduce visceral blood flow, induce ischemia, and cause
organ dysfunction.48 Intraabdominal pressure of 20 mmHg decreases mesenteric
arterial blood flow significantly. At an intraabdominal pressure of 40 mmHg, the pH
falls to levels indicating severe mucosal ischemia which may be as important as the
pulmonary, cardiac, and renal changes.44 In an experimental study, all viscera except
the adrenal glands showed a marked reduction in blood flow beyond that attributable
to the decrease in cardiac output.48 Caldwell and Ricotta found that the changes in
organ blood flow were more marked than could be accounted by changes in cardiac
output alone.48
Despite normal systemic hemodynamics, splanchnic ischemia may occur
with slightly elevated intraabdominal pressure. Such ischemia may be associated
with an increased incidence of multiple organ failure and mortality.59 Intestinal
ischemia has been reported during prolonged laparoscopy in patients with normal
central hemodynamics.60,61 Splanchnic hypoperfusion and gut acidosis commence at lower intraabdominal levels and long before the manifestations of
abdominal compartment syndrome become clinically evident.5 Intestinal lowgrade ischemia is seen at an intraabdominal pressure of 15 mmHg and is
associated with bacterial translocation.62
NEUROLOGIC ABNORMALITIES
Increased intraabdominal pressure elevates intracranial pressure and reduces cerebral
perfusion pressure.1,2,63 Bloomfield et al. also showed that the increased intracranial
pressure was due to elevated intrathoracic pressure.1 The change of intracranial
97
pressure is induced by elevated intrathoracic pressure and central venous pressure

(Figure 7.1). Intracranial pressure and hemodynamic parameters normalized when
pleural pressure was kept at atmospheric level.
Reduced intraabdominal pressure by decompression normalized intracranial
pressure in these experiments. In another study, sternotomy and pleuro-pericardiotomy prevented the rise of intracranial pressure.19 Therefore, patients with both
increased intraabdominal and head injury may be at risk for profound injury to the
central nervous system.
ABDOMINAL WALL ABNORMALITIES

The compliance of the peritoneal cavity is 20 times greater at atmospheric pressure
compared to that at an intraabdominal pressure of 40 mmHg.50 Laplace law may be
applied to the abdominal cavity. The tension of the abdominal wall is described by
the relationship T = p r. Tension of the abdominal wall (T) is directly proportional
to the intraabdominal pressure (p) and the radius (r) of the abdominal cavity.
Increased intraabdominal pressure may cause abdominal muscle ischemia, increased
risks for infection, and herniation.40
MEASUREMENT OF INTRAABDOMINAL PRESSURE

Intraabdominal pressure may be measured directly with an intraperitoneal catheter
attached to a transducer. Indirect methods to estimate intraabdominal pressure
include urinary bladder pressure, gastric pressure, and pressure in vena cava.
A grading system based on intraabdominal pressures has been proposed. Grade
I is intraabdominal pressure between 10 and 15 cm H2O, Grade II is 15 to 25 cm
H2O, and Grade III is between 25 and 35 cm H2O.16 This grading system has been
correlated to clinical findings and suggested treatment.
DIRECT MEASUREMENTS
Intraabdominal pressure can be measured directly by a fluid-filled intraperitoneal
catheter connected to a transducer or, if not available, a manometer.4,8,17,18,40,6467
Blunt techniques similar to measurements of intramuscular pressures may be
used.40,6466 The CO2 insufflators for laparoscopy can be used to automatically
increase and measure intraabdominal pressure.
URINARY BLADDER PRESSURE

Intraabdominal pressure may be indirectly determined by measuring urinary bladder
pressure by a Foley catheter.17 Bladder pressure closely reflects intraperitoneal pressure.68 However, patients with small neurogenic bladder or intraperitoneal adhesions
as well as patients with obesity, pregnancy, or ascites may give unreliable estimates
of intraabdominal pressure.20
The bladder is drained and then filled with 50 to 100 mL of sterile saline
through the Foley catheter. The tubing of the collecting bag is clamped. The
catheter is connected to a pressure transducer. The symphysis pubis is the zero
98
Zero level
FIGURE 7.2 Indirect determination of intraperitoneal pressure by measuring urinary bladder

pressure. The bladder is drained and then filled with 50 to 100 mL of sterile saline through
the Foley catheter. The tubing of the collecting bag is clamped. The catheter is connected to
a pressure transducer. The symphysis pubis is used as the zero level.
reference (Figure 7.2). The technique shows a high degree of correlation with
direct measurements of intraabdominal pressure up to 70 mmHg.43,68
INTRAGASTRIC PRESSURE
A nasogastric tube may be used to measure pressure in the stomach as an estimate
of intraabdominal pressure. Hydrostatic pressure can be obtained after installing 50
to 100 mL of saline in the stomach.18,69 A gastric balloon filled with air may also
be used for pressure recordings.70 Extracorporal transducers are leveled at the midaxillary line to avoid hydrostatic artifacts from the tubing. Human studies have shown
an acceptable correlation of gastric pressure to pressure in the urinary bladder.69,70
PRESSURE
IN THE INFERIOR
VENA CAVA
No human studies have validated its use. The method is associated with significant
risks. However, it has been shown in an experimental study that pressure in the
femoral vein catheter correlates well with intraabdominal pressure measured directly
and with urinary bladder pressure.71
CLINICAL MANIFESTATIONS
Symptoms of increased intraabdominal pressure include respiratory, cardiovascular,
and renal dysfunction (Figure 7.3). Trauma patients who require abdominal packing,
patients with coagulopathy, and those with profound hypothermia are at high risk.
In Stage I, the abdomen is swollen and the circumference is increased as a sign of
increased volume. The distended abdomen becomes tense. Venous stasis is seen in
the lower extremities. The symptoms of Stage I may start at an intraabdominal
pressure of 10 to 20 mmHg.16,59 In Stage II, the abnormally elevated intraabdominal
99
Abnormally elevated intraabdominal pressure
Elevation of diaphragm
Vascular compression
Organ compression
Cardiac
compression
Increased pressure
of intra- and retroperitoneal veins
Visceral ischemia
Renal
dysfunction
Increased venous pressure

and interstitial pressure
in the lower extremities
Increased intrathoracic pressure
Decreased
cardiac output
Increased intracranial pressure
Respiratory
failure
FIGURE 7.3 Algorithm illustrating how abnormally elevated intraabdominal pressure

induces renal dysfunction, respiratory failure, decreased cardiac output, and visceral ischemia.
pressure affects the microcirculation of the intra- and retroperitoneal organs. Progressive oliguria, in spite of adequate cardiac output, and hypoxia with respiratory
dysfunction evolve in the patient. In Stage III, symptoms of intra- and extraabdominal organs occur. These include respiratory, cardiovascular, renal, and visceral
dysfunction. Most studies of the relationship between elevated intraabdominal pressure and organ dysfunction have been performed on hemodynamically stable patients
or in animal experiments. They indicate that intraabdominal pressure exceeding 20 to
25 mmHg in trauma patients may need surgical treatment.
RESPIRATORY SYMPTOMS
Patients have difficulty breathing. They become tachypnoic. Most of them are critically ill and require artificial respiration. Increased intraabdominal pressure is associated with elevated diaphragm7,41 and increased pulmonary airway pressure, with
decreased arterial oxygen tension and hypercarbia. Pulmonary compliance is low
and patients require positive end expiratory pressure to maintain oxygenation.18
Chest x-ray shows small lung fields and elevated diaphragms.
CARDIOVASCULAR SYMPTOMS
Patients have metabolic acidosis, tachycardia, low stroke volume, and elevated
central venous pressure. The cardiac output decreases due to increased peripheral
resistance and due to decreased venous return (Figure 7.1). Pulmonary wedge pressure is increased. Large volumes may be contained in the lower limbs due to venous
stasis created by pressure on the inferior vena cava. Intraabdominal pressure of
14 mmHg increases the femoral venous pressure from 10 to 18 mmHg.54 This level
100
of pressure reduces or even eliminates pulsatility in the common femoral vein,

indicating proximal venous stasis.
RENAL
AND
VISCERAL SYMPTOMS
Oliguria and anuria occur when intraabdominal pressure exceeds 25 to 30 mmHg.

Prolonged low-grade visceral ischemia is associated with bacterial translocation,
sepsis, and multiorgan failure.
TREATMENT
Respiratory, cardiovascular, and renal dysfunctions are difficult to manage unless the
intraabdominal pressure is reduced.7,20 Surgical treatment of the abdomen by celiotomi
is the best way to normalize elevated intraabdominal pressure.19 Prophylactic mesh
fascial closure at the initial laparotomy may reduce the incidence of acute abdominal
compartment syndrome, adult respiratory distress syndrome, and renal failure. Abdominal decompression produces polyuria and improved creatinin clearance.
NONSURGICAL TREATMENT
Central venous pressure as well as pulmonary artery occlusion pressure (or pulmonary wedge pressure) are normal or elevated. Therefore, it is easy to assume that
the patient has an adequate volume of the intravascular space. However, cardiac
filling pressure to determine intravascular volume status is not reliable in these
patients.72 Patients with abnormally elevated intraabdominal pressure should be
treated by adding volume when their cardiac output is low.
Arterial blood gas measurements demonstrate hyperemia, hypercardia, and acidosis, which all reflect physiological derangement. Mechanical ventilation with a
positive end expiratory pressure inhibits metabolism of lactate.41,53 However, it may
cause further physiological abnormality if the increased intraabdominal pressure
remains elevated. Intravascular volume should be restored and oxygen delivery
maximized.47 Hypothermia and coagulopathy must be corrected.
SURGICAL TREATMENT
Surgical and nonsurgical treatment for acute abdominal compartment syndrome must
be executed simultaneously. It has been suggested that an urinary bladder pressure
exceeding 25 mmHg associated with unexplained oliguria is an indicator for decompression.17,19 Surgical treatment is conducted by abdominal decompression. After
decompression, the abdomen is left open. Decompression of the abdomen is associated with a substantial improvement in survival rates. Escharotomy or tangential
excision of abdominal burns may be helpful in burn patients with abdominal scars.39
Results
Surgical decompression of the peritoneal cavity reduces intraabdominal pressure
and reverses this derangement.19,73 The central venous pressure, urinary output,
101
ventilatory pressure, carbon dioxide tension, and oxygenation are normalized. The
decompression improves acute respiratory failure.7,18,43 Abnormally elevated peak
airway pressures (>80 cm H2O) may improve to normal levels.16 The elevated
pulmonary airway pressure and PaCO2 normalize soon after abdominal decompression. However, pulmonary oxygenation may take 18 to 36 h to return to normal.7
Renal function returns to normal following decompression of patients with increased
intraabdominal pressure due to postoperative hemorrhage.28
Adverse effects of surgical decompression have been described. These
include severe hypotension immediately after the abdominal cavity is
opened.3,5,25 This may be explained by a sudden decrease of systemic vascular
resistance or by a reperfusion syndrome.3 Therefore, volume loading before
abdominal decompression is advocated.5,74 Anaerobic metabolites reach circulation by the reperfusion. Cardiac asystole following abdominal decompression
has been described in one fourth of the patients with acute abdominal compartment syndrome.3 Asystole has been reported in 12 to 25% of the patients
following abdominal decompression.5,74
Wound Closure
Primary closure of abdominal wall may not be possible in patients with massive
visceral edema and large intra- and retroperitoneal hematoma. When the abdomen cannot be closed without acceptable tension, it must be left open. The skin
may be closed by sutures or towel clips to protect the bulging viscera. It may
be covered with sterile plastic drape.1 Secondary wound closure may be performed 7 to 10 days following the primary insult when edema is reduced and
renal function normalized.5 A silicon rubber sheet can be used to close abdominal
wall in patients where primary abdominal closure was impossible or where it
resulted in compromise in respiratory or renal function.57 Synthetic mesh grafts26
and plastic or rubber sheets have been used to close and reconstruct abdominal
wall.3,75
CHRONIC ABDOMINAL COMPARTMENT

SYNDROME
In patients with gradual increase of intraabdominal pressure, various organ systems
are able to compensate for the increased intraabdominal pressure. The acute symptoms from multiple organs do not occur in these patients. The chronically elevated
intraabdominal pressure may give rise to recurrent symptoms in these patients, which
could be labeled chronic abdominal compartment syndrome.
Chronic elevation of intraabdominal pressure, as seen in obese patients, may
produce obesity hypoventilation syndrome. Chronic elevation of intraabdominal
pressure has been suggested to cause benign intracranial hypertension in excessively obese patients.76,77 Obese patients may have elevated intraabdominal pressure, which increases pleural pressure, cardiac filling pressure, and impedes
venous return from the brain, leading to intracranial pressure associated with
pseudotumor cerebri.77
102
SUMMARY
Acute abdominal compartment syndrome is caused by abnormally elevated
intraabdominal pressure. Elevated pressure induces dysfunction of intraabdominal
and extraabdominal organs. The three pathogenetical mechanisms that cause the
syndrome are increased volume of the intraperitoneal contents, external compression, and decreased size of the intraperitoneal cavity. Intraabdominal pressures of
10 to 25 mmHg decrease cardiac output and venous return from the lower extremities, and induce respiratory, renal, and visceral dysfunction. The intrathoracic and
intracranial pressures increase. Intraabdominal pressure may be directly determined by an intraperitoneal catheter or indirectly by urinary bladder pressure
measurements. Abnormally elevated intraabdominal pressure, estimated as urinary
bladder pressure exceeding 25 mmHg, associated with unexplained oliguria is an
indicator for decompression. The syndrome is fatal if left untreated. Surgical
decompression by celiotomi reverses the symptoms and normalizes the circulation
and the function of abdominal organs.
REFERENCES
1. Bloomfield, G.L., Dalton, J.M., Sugerman, H.J., Ridings, P.C., DeMaria, E.J., and
Bullock, R., Treatment of increasing intracranial pressure secondary to the abdominal
compartment syndrome in patients with combined abdominal and head trauma, J.
Trau., 39, 1168, 1995.
2. Josephs, L.G., Este-McDonald, J.R., Birkett, D.H., and Hirsch, E.F., Diagnostic
laparoscopy increases intracranial pressure, J. Trau., 36, 815, 1994.
3. Morris, J.A., Eddy, V.A., Blinman, T.A., Rutherford, E.J., and Sharp, K.W., The staged
celiotomy for trauma: issues in unpacking and reconstruction, Ann. Surg., 217, 576,
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5. Ivatury, R.R., Diebel, L., Porter, J.M., and Simon, R.J., Intraabdominal hypertension
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7. Fietsam, R., Villalba, M., Glover, J.L., and Clark, K., Intra-abdominal compartment
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8. Emerson, H., Intra-abdominal pressure, Arch. Int. Med., 7, 754, 1911.
9. Marey, Physiologie mdicale de la circulation du sang, Paris, 1863.
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33. Maxwell, R.A., Fabian, T.C., Croce, M.A., and Davis, K.A., Secondary abdominal
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49. Toomasian, J.M., Glavinovich, G., Johnson, M.N., and Gazzaniga, A.B., Hemodynamic changes following pneumoperitoneum and graded hemorrhage in the dog, Surg.
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Positive end expiratory pressure with increased intra-abdominal pressure, Surg. Gyn.
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106
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Ischemic Contractures
INTRODUCTION
Untreated acute compartment syndrome evolves to ischemic contracture of affected

tissues. After 4 h of total ischemia, 5% of muscle bers become necrotic. After 8 h
of ischemia, all muscle bers are damaged. The muscle becomes brotic. This leads
to loss of joint motion and imbalance of forces acting over the joint. Peripheral
nerves may become compressed secondarily by the muscle brosis, which may
induce further neuromuscular dysfunction. The limb dysfunction induces disability
(decreased activity) and handicap (decreased participation). The aims of the clinical
investigation of these patients are to document which muscles and nerves are affected
and to what extent the tissues are damaged. The aim of this chapter is to discuss
general principles of diagnosis, classication, and treatment of ischemic muscle
contractures. Congenital and nonischemic reasons for contractures such as neuromuscular and inammatory diseases are not included.
DEFINITIONS
Volkmanns contracture is a limb deformity that represents one of the nal stages
of muscle and nerve brosis following an untreated acute compartment syndrome.
Muscular contracture may also occur as a secondary response to primary muscle
ischemia or from a direct irreversible ischemic nerve injury.
In papers prior to 1972, acute compartment syndrome was classied as Volkmanns contracture in the Index Medicus. Acute compartment syndrome was classied as early contracture and the established ischemic contracture as late contracture.1 Many cases previously termed as early contracture are today diagnosed as
acute compartment syndrome.
BACKGROUND
Von Volkmann rst described the clinical entity in 1881.2 He proposed that the
syndrome was caused by tight dressings (external compression) of traumatized limbs.
The contracture was considered to be due to ischemia caused by prolonged blocking
of the arterial supply. Von Volkmann also thought that the simultaneous venous stasis
accelerated progress of the paralysis. The contracture was described in terms of rigor
mortis. Today, the contracture is regarded as the result of ischemic injury to selective
tissues. Therefore, the condition will be labeled as ischemic contracture in this
chapter. The ischemic contracture of Volkmann may be regarded as the local tissue
complications following an untreated acute compartment syndrome.
107
108
EPIDEMIOLOGY
In a study on tibial shaft fractures, 1% of the patients with minor severity of injury
and 22% of patients with major injury had signs of contracture.3 In that study, patients
with severe limitations of ankle and foot movement comprised one third of the
patients with disability. Forearm fractures account for 15%4 to 20%5 of contractures.
In the review of Volkmanns ischemic contracture seen at the Mayo Clinic during
1935 to 1954, the time elapsed from injury until the patient was seen at the clinic
varied from 4 h to 27 years.1,6 Prior to 1935 the incidence of ischemic contracture
was 0.18 per thousand new registrants. From 1935 to 1954, the incidence decreased
from 0.08 to 0.03 per thousand new registrants.5 Later, soft tissue injuries and crush
injuries without associated fractures represented a larger proportion of cases.
Ischemic contracture may be the reason for persistent stiffness of the ankle and foot
in 1 to 10% of these patients.
ETIOLOGY AND PATHOGENESIS

Every acute compartment syndrome that is left untreated evolves into an ischemic
contracture. Direct local injury, proximal vascular injury, arterial occlusion, or
any combination of a no-ow situation (Figure 8.1) may initialize ischemic
contracture. A direct injury leading to impairment of the arterial supply of a
specic muscle may also induce a contracture state. Venous obstruction is an
important pathogenic factor.7 In experiments where only the veins were tied,
pathologic changes were found in every instance.8 Within an hour after vein
Proximal vascular injury or
arterial occlusion
Direct local injury
Any no-flow situation
Prolonged ischemia
Postischemic reperfusion
Abnormally elevated intramuscular pressure
Nerve injury
Muscle injury
Ischemic contracture
FIGURE 8.1 Pathogenesis of ischemic contractures following trauma is abnormally elevated

intramuscular pressure. Muscle contracture may be induced by injury to muscle and nerve.
109
obstruction, the muscle became swollen, hard, and dark blue. Contracture followed always after these experiments. Experimentally induced contracture after
only arterial ligature appeared later than that produced by acute venous obstruction.8 Other pathogenetical mechanisms suggested for ischemic contracture
include the theory of spasm of arteries and their collateral branches induced by
the sympathetic nervous reex system.
Muscle contracture may follow in patients with fractures treated without bandages. It may occur in patients with tibial fractures without pain. The risk for
contracture increases if patients are not treated within 12 to 24 h of ischemic
muscular pain. Muscle contracture may result from direct brosis of the small
muscles of the hand following burn injuries.9
Direct injury of the tissues in a compartment may induce ischemia due to an
abnormally elevated intramuscular pressure. Arterial injury or arterial occlusion may
give ischemia distal to the lesion. In these cases, tissue pressure is most often normal
initially in the affected part of the limb. However, following restoration of the arterial
occlusion, a reperfusion syndrome may occur, which may induce abnormally
increased intramuscular pressure. Direct ischemic injury to the nerve tissue may also
induce muscular contracture.
The pull on plantar exor muscles by dorsiexion of the ankle joint increases
intramuscular pressure to levels that may induce ischemia in the posterior compartment of the leg.10,11 Immobilization of the leg and foot in plaster cast, keeping the
ankle joint in slight plantarexion, diminishes the risks for increased intramuscular
pressure in all compartments.11,12
PATHOPHYSIOLOGY
Ischemic insults to muscle tissue may recover completely and induce gangrene or
contracture. Gangrene involves all tissues including the most distal. In contrast,
contracture is due to ischemia of selective tissues such as muscles and nerves of the
affected compartments. Tissues distal to the compartment are not affected initially.
They are not ischemic.
Pathologic changes of muscle contracture include edema, disappearance of
nuclei and sarcolemma, loss of muscle striation, and hyalin degeneration with atrophy.13 Muscle necrosis may be partly reversible if the local circulation can be restored
before brous replacement has occurred.14 Five percent of the muscle cells become
necrotic after 4 h of total ischemia. After 8 h of total ischemia, 100% of the cells
are necrotic.15 They may become dysfunctional due to the proximal nerve and muscle
insult. Some areas of the necrotic muscle may regenerate whereas others heal by
brosis, which gradually causes a contracture. Skeletal muscle bers may regenerate
from satellite cells of a dying ber if the basal lamina of the ber is intact. The
mechanism for activation is autonomous to the ber and can occur without nerve
or blood supply.16 The number of satellite cells decreases with age and the capacity
to regenerate skeletal muscle also appears to decrease with age. When muscles
become ischemic, they lose their elasticity by degeneration of the fascicles. In the
residual state, the muscle becomes rigid and contracted.13
110
GENERAL PRINCIPLES OF DIAGNOSIS,

CLASSIFICATION, AND TREATMENT
SYMPTOMS
Patients with ischemic contracture may experience pain, paresthesia, hypoesthesia,
and paresis. They also experience cold, cyanosis, swelling, and joint stiffness. The
range of motion amplitude is decreased. Muscles become hypotrophic and the
affected limb is weak.
Some patients may recall severe pain in their initial history of trauma. The pain
may have been resistant to pain medication during that time period. Some patients
may have experienced pain for several weeks or months after the acute untreated
compartment syndrome.17
CLINICAL FINDINGS
The purpose of the clinical investigation is to determine the extent of muscle and
nerve damage. Findings at clinical investigation include loss of motor and sensory
function, decreased range of motion, and deformities of ngers and toes. These
ndings form the basis for choice of treatment. Patients may have difculties in
reaching a neutral position of the joint. Subluxation of involved joints may occur.
After the initial stages of the syndrome, the clinical picture can vary considerably.
Patients express difculties to grip with their hands or stand on their feet.
Muscle Tissue
The retraction of exor muscles at the distal joints in the limbs is the most striking
feature of ischemic contracture. The tenodesis effect implies that a contracted nger
or toe is extended if the wrist or ankle joint is exed (Figure 8.2). Conversely, if the
wrist or ankle joint is extended, the position of the nger or toe becomes more
exed. The involvement of nerve damage contributes to the clinical variety of
functional impairment. Muscular imbalance develops by long-standing muscle palsies. This may create articular stiffness and subluxation of the involved joints. The
active and passive range of motion of joints is reduced.
Nerve Tissue
Nerve lesions represent another important feature of the clinical picture. This
includes motor decit of the leg and foot muscles. Electromyographic investigation
is a valuable aid in difcult cases. Sensory decits are seldom present without motor
involvement. In their series, 60% of patients with motor decit had normal sensitivity.18 Muscular hypotrophy, dry cyanotic skin, and dystrophic nails are common
ndings in these patients.18 The sudomotorfunction is impaired.
CLASSIFICATION
Classication of contractures is essential in determining the method and timing of
treatment. Several classications have been suggested. Contractures have been
111
FIGURE 8.2 Example of ischemic contracture of the extensor muscles of the anterior compartment of the left leg in a patient with acute anterior compartment syndrome 1 year earlier.
The extensor hallucis longus muscle is brotic. When the patient plantarexes the foot, the
metatarsophalangeal and interphalangeal joint of the left big toe becomes hyperextended
(tenodesis). The ankle joint exion is impeded.
classied into three grades19 or four grades1 based on severity. They have also been
classied into three types,20 four types,21 or ve stages18 based on severity and tissue
involvement. Classication must be based on a thorough clinical investigation and
is most important before determining treatment. A three-grade general classication
of ischemic contractures mild, moderate, and severe contractures has been
used in this chapter whenever possible.
Mild Contracture
This is a localized type in one or a subtotal number of muscles in the compartment.
Force generation of affected joints is normal or slightly decreased. There is normally
no sensory dysfunction. As a sign of muscular retraction, a tenodesis effect is always
present (Figure 8.2).
112
Moderate Contracture
Most muscles of the compartment are involved, both deep and supercial muscles.
All ngers or toes are contracted. Sensory dysfunction is common. Articular stiffness
due to secondary contractures of joint tissues is mild.
Severe Contracture
All muscles are necrotic and sensory dysfunction is severe. Secondary joint contractures are commonly seen, with contracted capsulae and ligaments. Articular
stiffness due to secondary contractures of joint tissues is severe. The joint forces are
not balanced around the neutral axis, which leads to subluxation and joint deformation. Dystrophic changes of other tissues such as skin and nails are seen.
TREATMENT
The overall goal of treatment is to regain active and passive range of motion around
the neutral position of the joint. This includes the ability of patients to stand on
plantigrade feet, to participate in common activities of daily living, and to use the
pinch and grasp grips of their hands.
The principles for treatment of the upper and lower limbs are basically the same
and may be divided into three phases. The rst phase is treatment by physiotherapy
and by supportive and corrective orthoses. This is achieved by serial casting or
dynamic splinting, or both. Often, patients need night splinting after the contracture
has been corrected. During this treatment, patients with sensory nerve dysfunction
have increased risks of developing skin ulcerations due to pressure. Muscle strengthening is an important part of the exercise program. Treatment by growth hormone
may increase growth of regenerating skeletal muscle after ischemic necrosis and
diminish atrophy of skeletal muscle after denervation.22
In the second phase, deformities are corrected by surgery of soft tissues. More
severe contractures that are not responsive to the methods previously described
may need surgical treatment such as lengthening or transfers of tendons. Nerve
compressions due to brotic muscles giving sensory or motor dysfunction should
be treated by decompression as soon as possible. Expected results following
decompression of nerves include increased sensitivity, increased muscle strength,
and decreased pain.
The third phase involves corrective bone and joint surgery as well as soft tissue
releases. The best time for surgical treatment is when the patient has had the peak
recovery, usually 3 to 6 months from the initial trauma. Delaying surgery for more
than 1 year is seldom necessary. In the following section, symptoms, clinical ndings,
and general principles of treatment of muscles and nerves of separate compartments
of the upper and lower extremities is discussed.
CONTRACTURES OF LEG MUSCLES

The relative involvement of different leg compartments and the degree of muscular
contracture in each compartment create a variety of different clinical pictures. There-
113
fore, clinical ndings and treatment of contracture in each of the main four compartments in the leg are described separately. Muscular retraction may be demonstrated by measuring the total passive range of motion decit. The total decit is
the clinical reection of the muscular retraction in the leg. The severeness of the
contracture can be estimated by range of motion scores of involved joints. Stiffness
of the foot and ankle correlate with the severity of the leg injury and occur in about
20% of major injuries.3 One third of patients with limitations of foot and ankle
movement had clinical evidence of ischemic contracture in that study.
In most patients, contractions affect mixed compartments. Therefore, the treatment must be individualized. Many of the patients need complex surgical procedures
including tendon transfers, tenotomies, and arthrolysis to gain improved function.
Arthrodesis of selected joints may be necessary.23 The goal of the treatment is to
regain active and passive range of motion around the neutral position of the involved
joints. This includes the ability of the patient to stand on a plantigrade foot. In severe
cases, a derotating three-dimensional wedge osteotomy of the distal part of the tibia
has been suggested.24 Nerves entrapped by brotic tissue must be decompressed
early in the rehabilitation period.
CONTRACTURE
OF THE
ANTERIOR COMPARTMENT
Symptoms
Patients experience decreased ability to dorsiex the ankle joint and toes. They have
gait difculties due to a drop foot. Plantarexion of the ankle joint is diminished.
The toes are painful and have decreased range of motion.
Clinical Findings
Patients may have sensory dysfunction over the rst interdigital cleft. The extensor
muscles may be weak. During maximal plantarexion, the big toe extends as a sign
of tenodesis (Figure 8.2). This is also true for passive exion of the ankle joint.
Treatment
In mild cases, a splint may be sufcient. In more severe cases, the posterior tibial
tendon may be transferred through the interosseous membrane to the dorsum of the
foot. The tendon is transected at its insertion into the navicular bone. It is retracted
proximally and brought anteriorly through the interosseus membrane. The distal
aspect of the tendon is attached to the middle cuneiform bone through a separate
incision.25 An alternative method is to transfer the peroneus longus or brevis muscle
to Os cuneiforme III23 or cuneiforme II.26 However, this alternative is often not
available because the peroneal muscles are also affected in many of the patients with
contracture of the anterior compartment.
Reconstruction with the peroneus longus tendon is an alternative for patients
with no remaining muscles in the anterior compartment. The tendon is brought
through the anterior intermuscular septum and transferred to the tendons of the
tibialis anterior muscle and to the long extensors of the toes.27
114
CONTRACTURE
OF THE
LATERAL COMPARTMENT
Symptoms
Patients experience local pain and sensory dysfunction of the supercial peroneal
nerve. The contracture results in a supination of the ankle joint due to forces
generated by the posteromedial structures of the leg.
Clinical Findings
Patients may have sensory dysfunction over the dorsum of the foot, except for the
rst interdigital cleft. The peroneal muscles are weak.
Treatment
Patients with mild symptoms are treated by a splint. Partial transfer of the anterior
tibial tendon to the lateral part of the dorsum of the foot or to the peroneus brevis
tendon insertion may restore balance of the ankle joint.
CONTRACTURE
OF THE
POSTERIOR COMPARTMENTS
Symptoms
Patients complain of painful rigid toes and pain in the forefoot. Patients may have
exion contractures of the toe joints, a cavus foot, and a xed equinovarus deformity.
The toe deformities, which include claw toes or mallet toes, are painful and may
create skin problems. The ankle joint hurts.
Clinical Findings
Patients have a short cavus foot with clawing of the toes. They may have an
equinovarus deformity of the forefoot (Figure 8.3 and Figure 8.4). The distance
between the lateral malleolus and the Achilles tendon may be shorter.24 This may
be explained by dorsiexion of the talocrural joint combined with adduction in the
midtarsal joint. This angulation forces the patient to rotate the leg outward to parallel
the feet during walking (Figure 8.3 and Figure 8.4).
Involvement of the distal part of the deep posterior compartment leads to claw
toes,26 due to contracture of the exor hallucis longus and the exor digitorum longus
muscles. When all muscles of the supercial and deep posterior compartments are
involved, the foot shows a xed equinovarus deformity.
Contracture of the posterior tibialis muscle causes a medial and plantar pull on
the navicular bone. These forces induce exion contracture in the talocrural joint.24
The active and passive range of motion is reduced. The subthalar joints may be
completely rigid, and the navicular and cuboid bones may be subluxated. The talus
and calcaneus bones are dorsiexed in these patients. If no weight bearing is allowed,
there is no counterforce to the pull of the tibialis posterior muscle. This effect will
also be strengthened by contracture of the exor hallucis longus and exor digitorum
muscles, which are responsible for the toe deformity.
115
FIGURE 8.3 Ischemic contracture following untreated acute compartment syndrome of the
left leg. The left side shows a short cavus foot with an equinu-varus deformity. The distance
between the lateral malleolus and the Achilles tendon (black bar) is shorter. (See color insert
following page 106.)
Treatment
The aims of the treatment are to restitute nerve function, release joint contractures,
and replace lost muscle function to balance the forces over the ankle joint. Treatment
must be individualized and may include neurolysis; tendon release; and lengthening,
tendon transfer, arthrolysis, and arthrodesis.
Impaired passive dorsiexion of the ankle joint may be increased by Z-platy of
the Achilles tendon. This may be combined with capsulotomy of the ankle joint and
lengthening of other exor tendons. Claw toes and mallet toes may be treated by
tenotomies of the exor hallucis longus and exor digitorum longus tendons. In
addition to soft tissue releases, correction by a wedge osteotomy of the foot may be
a necessary treatment in patients with xed deformation of the foot. In severe cases,
Karlstrm et al. suggested treatment by a derotation three-dimensional wedge osteotomy of the distal part of the tibia.24
CONTRACTURES OF FOOT MUSCLES

Untreated acute compartment syndromes of the foot or foot and leg compartments
may induce complex posttraumatic deformities. This has been labeled the short
116
FIGURE 8.4 Mild claw toe deformities of dig. II to IV in a patient with ischemic contracture
of the exor digitorum longus muscle and intrinsic dysfunction. Soft tissues along the longitudinal arch are hypotrophic. The foot is shorter and has a cavus deformity. (See color insert
foot syndrome. It includes a contracted pes equinovarus foot with clawing of the
toes. Contracture of the short toe exors of the foot is seen after fractures of the
calcaneus and crush injury of the foot. Assessment by sonography or MRI may
demonstrate scarred, necrotic musculature in the involved compartments. The muscular imbalance over the affected joints forces them into subluxation or luxation.
Treatment may require complex soft tissue release, muscle and tendon transfer,
lengthening of tendons, and release of intrinsic muscles. The etiology of clawed toes
was not known (or idiopathic) in 80% of patients in an operated series.28
ANATOMY
Four to nine anatomical compartments of the foot have been described (Figure 8.5).
Each of the compartments may develop brotic muscle tissue in response to untreated
acute compartment syndrome or injury. The intrinsic muscles of the foot ex the
metatarsophalangeal joints and extend the proximal and distal interphalangeal joints.
Many factors such as extent of muscle necrosis in the foot and leg and nerve
dysfunction determine whether the toes will be clawed or develop another deformity.
Furthermore, the clinical picture of the foot deformity may be more complicated
when contracture of leg muscles coexists.
SYMPTOMS
Patients with ischemic contracture of foot muscles experience pain, paresthesia,
hypoesthesia, and paresis. They also experience swelling and stiffness of toe joints.
The range of motion amplitude of the foot and toe joints is decreased. Claw toe is
117
Interossei (four)
Medial
Lateral
Adductor
Superficial
FIGURE 8.5 Compartments of the foot. Nine compartments of the foot have been described.
The calcaneus compartment is located more dorsal, closer to the calcaneal bone, compared
to this section of the foot.
a symptom and not an entity. Clawing of the toes implies that they are painful and
can no longer full their normal dynamic function.
CLINICAL FINDINGS
Three types of toe deformities are dened. The terms hammertoe and claw toe have
been used interchangeably in the literature. Claw toe has been used to describe the
distal changes in patients with neuromuscular diseases. The claw toe deformity
involves the metatarsophalangeal joint, which is hyperextended (Figure 8.6). Hammertoe is used to describe an abnormal exion posture of the proximal interphalangeal joint in one or more of the lesser four toes. The deformity is xed. It is not
possible to passively correct it to the neutral position. Mallet toe is a exion posture
of the distal interphalangeal joint.
The clinical manifestation is clawing of the toes or formation of hammer toes.
Hammer toes may be due to untreated compartment syndrome of the intrinsic muscles
of the foot.23 The loss of intrinsic muscle function leads to muscle imbalance over the
toe joints. Patients with claw toes (intrinsic minus deformity) have extension of the
metatarsophalangeal joint, exion of the proximal interphalangeal joint, and extension
of the distal interphalangeal joint (Figure 8.6). The toe deformity is similar following
contracture of the exor digitorum longus, but the distal interphalangeal joints are
exed and the other joints of the toes may even be in neutral position.23 Curly toes
differ from claw toes by having the metatarsophalangeal joint in a neutral position. A
cavus foot deformity may be due to both intrinsic and extrinsic contracture.
TREATMENT
Treatment of the contracted foot includes complex soft tissue release, muscle and
tendon transfer, tendon-lengthening procedures, and intrinsic releases to correct the
118
A.
B.
C.
FIGURE 8.6 Three types of toe deformities may be found at clinical investigation. (A) The
hammer toe deformity is due to contracture of the intrinsic (short exor) muscles of the foot.
(B) The claw toe deformity is due to a mixed contracture of the intrinsic and extrinsic exors.
(C) The mallet toe is due to isolated contraction of the extrinsic muscles of the foot (long exors).
deformity.23 Pes cavus may be treated by a wedge osteotomy. Toe deformities can
be treated with conventional methods for foot reconstruction.
CONTRACTURE OF THIGH MUSCLES

Most patients described in the literature are young children who developed
contractures following multiple intramuscular injections in the thigh.2931 Causes
other than abnormally elevated intramuscular pressure may have induced the
contracture in these cases. The contracture may appear in three forms: the vastus
lateralis form, the rectus femoris form, and a combined form. The symptoms
and clinical ndings vary according to the degree to which the different muscles
are involved.
SYMPTOMS
Patients complain of limited exion of the knee joint due to contracture of the
quadriceps muscles. They experience pain on walking during an extended period of
time, abnormal gait pattern, and inability to sit cross-legged and in the Japanese
style.32 Patients have difculties in squatting. Contractures of selective thigh muscles
may induce anterior knee pain due to patellar luxation or subluxation.33
119
FIGURE 8.7 The Elys test. During passive knee exion in a prone patient, the pelvis begins
to elevate from the table. This is due to a contracted rectus femoris muscle. The angle of knee
exion at which this occurs is expressed as the pelvic elevation angle.
CLINICAL FINDINGS
Flexion of the knee joint is restricted if the vastus lateralis is affected. If the rectus
femoris muscle is affected, knee exion on full extension of the hip joint is
restricted.32 Patients have a positive Elys test, which means that the pelvis will
rise off the table or bed on knee exion in the prone patient. The angle of knee
exion when the pelvis is elevated from the table is dened as the pelvis elevation
angle (Figure 8.7).
The severity of rectus femoris contracture may be graded into four stages
according to the knee total range of motion. Stage I includes patients with less than
31, Stage II a range of motion between 31 and 60, Stage III between 61 and 90,
and Stage IV more than 90. The contracture is more severe when the angle is smaller.
By measuring the range of motion of the knee, rst with the hip exed and then
again with the hip extended, the contribution of the rectus femoris muscle to the
contracture can be demonstrated and evaluated.34
TREATMENT
Patients with a mild contracture may be treated by stretching during the early
phase of the condition. In established moderate contractures, surgical treatment is
indicated. In severe cases, passive stretching and physiotherapy are unlikely to
produce lasting improvements.30,35
Surgical treatment for quadriceps contracture includes proximal muscle release,
Z-plasty of the rectus femoris muscle, VY lengthening, and distal releases of the
quadriceps muscles.
Proximal Release
Several alternatives to performing proximal releases are described.35 It may be
performed through a SmithPedersen anterior ileofemoral approach. Division of
the fascia lata and proximal release of the quadriceps muscles along the tro-
120
A.
B.
FIGURE 8.8 Drawing of the surgical procedure of proximal release of quadriceps muscles.
(A) Skin incision. (B) The iliotibial band and tensor fasciae latae are cut. Vastus lateralis is
detached from its origin at the greater trochanteric line and allowed to slide distally. The
rectus femoris muscle may be released through the same incision. (Redrawn after Sengupta,
S., J Pediat. Orthop., 5, 187, 1985.)
chanteric line and lateral intermuscular septum are performed (Figure 8.8). With
the subject in supine position, a longitudinal incision is made over the brotic
part of the rectus femoris muscle.36 With the affected leg hanging down from
the operation table and creating tension of the muscles, a transverse incision is
made in the brotic part of the rectus femoris muscle. Additional transverse
incision of the brotic iliotibial muscle and other quadriceps muscles may be
performed while the knee is further exed. In severe cases, the procedure is
combined with release of the sartorius muscle and the tensor fasciae lata.37
Postoperatively, the hip is kept fully extended and the knee exed 90 in a spica
for 2 to 3 weeks.
After surgery, the knee is kept in maximal exion for 3 or 4 weeks in a plaster
cast. When the cast is removed, vigorous quadriceps exercises are important to
improve the extensor lag. Knee-stretching exercises must be continued throughout
the growing period.
Z-Lengthening
The importance of Z-lengthening of the rectus femoris muscle has been emphasized.29 Satisfactory active and passive range of motion following Z-plasty was
described in three cases. After surgery, patients were immobilized in a cast for
6 weeks.
VY Lengthening
VY lengthening of the quadriceps muscle tendon according to Thomsen procedure
is an alternative method if all quadriceps muscles are affected. The method is not
suitable in patients with selective contractures.
121
Distal Quadricepsplasty
This is a soft tissue operation in the distal one third of the thigh. An incision is made
along the lateral border of the rectus tendon in the distal third of the thigh. The
fascial sleeve is opened. Attachment of the fascia lata to the patella is divided.33
RESULTS
AND
COMPLICATIONS
Sasaki et al. saw nerve palsies in 15% of the patients.32 The femoral lateral cutaneous
nerve may be affected in patients treated by release of the pelvic origin and the
saphenous nerve after release of the muscle belly.32 Other complications include
patellar luxation. Williams described patients who could not ex their knee joint
more than 30 if the patella was forcefully held in midline.33 Further knee exion
was possible only if the patella was allowed to dislocate.
Jackson and Hutton compared treatment by proximal release and distal quadricepsplasty.34 Patients treated by proximal release showed better results. Knee
exion was 80 and no knees demonstrated an extension lag. Distal quadricepsplasty gave an extension lag in 70% of patients after an average follow-up of 10
years. It has been concluded that surgery should be avoided in patients who are
younger than 5 years,32,38 and it has been recommended in patients over 6 years32
and 10 years of age.38 Following these procedures, knee exion may increase by
40 to 80.
CONTRACTURE OF GLUTEAL MUSCLES

This is an unusual condition. Patients may experience symptoms of sciatica without
low-back pain. They have atrophy of the buttock. In children, range of motion of
the hip joints is severely decreased in exion and abduction. Based on data from
clinical investigation and neurography, it is possible to classify stages of severity of
the contracture.
Tight structures may be surgically released. A normal range of motion was
reported 1 year after surgery in children.39
CONTRACTURE OF HAND MUSCLES

Bunnell rst described ischemic contracture in the hand in 1948.40 It can involve
the whole hand or isolated compartments of the hand. Selective paralysis may be
difcult to detect early. Often, hand ischemia is a part of a more complex clinical
picture including compartment syndrome of the forearm, stretch injury of the brachial plexus, arm fractures, and limb ischemia due to prolonged external compression
in patients with drug-induced coma or crush injury. The intrinsic muscles of the
hand participate in a complex nger joint motion with the extrinsic tendon system.
They are most important to maintain a normal balance over the nger joints. Ischemic
contracture of the muscles result in a signicant loss of hand function. Superimposed
nerve damage will add to hand dysfunction. Ischemic contractures of the hand may
be classied as mild, moderate, or severe.40
122
ANATOMY
The hand has six to ten compartments. There are four dorsal and three volar interosseus muscles of the hand. Each dorsal interosseus muscle has two heads, except
the third, which has one head. The lumbrical muscles arise from a tendon and insert
onto the deep exor tendon.
SYMPTOMS
Patients may complain of pain, weakness, numbness, stiffness, and anesthesia. They
may experience difculties in grasping things of certain sizes. The range of motion
of the joints does not allow the hand to be opened sufciently for grasping.
CLINICAL FINDINGS
Muscle Tissue
In late cases with brosis and shortening of the interossei muscles, the metacarpophalangeal joints are exed and the interphalangeal joints are extended. This
condition has been labeled intrinsic plus position.41 The hand assumes the same
position which hyperactivity of the intrinsic muscles would induce. The end result
is a disabling deformity with loss of the pinch and grasp grips.
The intrinsic test is useful for diagnosis of intrinsic contracture in the
hand.40,42 If the metacarpophalangeal (MCP) joint is passively held in extension,
the interphalangeal joints lose exion ability (Figure 8.9). Active and passive
exion ability of the interphalangeal joint increase if the MCP joint is held in
exion. The proximal interphalangeal (PIP) joint exion will be less when the
metacarpophalangeal joint is extended compared to when it is exed. This is a
positive intrinsic test (Figure 8.8). If there is an extension contracture of the PIP
A.
B.
FIGURE 8.9 The intrinsic tightness test is positive if the interphalangeal joint has decreased
range of motion when the MCP joint is held in extension (A) and increased range of motion
when the MCP joint is exed (B).
123
joint due to tight extensor tendons, PIP joint exion will be greater when the
MCP joint is exed. However, capsular or intraarticular adhesions may limit the
range of motion of the proximal interphalangeal joint and thereby an underlying
intrinsic contracture.
Nerve Tissue
Sensation in the digits is usually normal. However, if the brosis involves the carpal
and Guyons tunnel, compression of the median and ulnar nerves may result in
sensory loss as well as motor dysfunction.
TREATMENT
In mild cases of interosseus contracture, an elastic splint extending the MCP joints
may be enough.40 Several surgical methods have been described, including
interosseous stripping, sectioning of the lateral bands, and release of the extensor
component of the intrinsic muscles on the interphalangeal joint. The aims of the
procedures are to restore the pinch and grasp functions, preserve nger extension
and exion, as well as abductionadduction functions of the intrinsic muscles at the
MCP joints.42
Interosseous Stripping
All intrinsic muscles are detached from the carpal bones with small periosteal
sleeve.40 The hand is immobilized in the claw hand position, that is, extended MCP
joints and exed IP joints until muscles are reattached in the more distal site.
However, the functional results have been reported as inferior.42 This operation is
suitable for patients with moderate contractures. The prerequisite to perform this
operation is that the intrinsic muscles are not too brotic.
Sectioning of Lateral Bands
In severe cases where the intrinsic muscles are too brous to function, Bunnell
recommended tenotomies of the lateral bands.40 The skin incision is made over the
dorsal aspect of the three nger webs. It may be necessary to cut collateral or volar
ligaments as well. The procedure is less traumatic. Recurrences of the deformity
have been reported.42
Release of Extensor Component
Littler modied Bunnells method of lateral band section by releasing the extensor
component of the intrinsic muscles on the interphalangeal joint.43 The exor
component was preserved on the MCP joint. The extensor hood at the MCP joint
consists of three structures: the tendon to the long extensor muscles, the transverse
bers, and the oblique bers of the intrinsic muscles. The oblique bers extend
the interphalangeal joints. By excising the oblique bers, the extensor contracture
of the proximal interphalangeal is released. The transverse bers may still preserve
their exion action on the MCP joints, which will prevent hyperextension in MCP
124
joints. Compensation for intrinsic muscle loss is possible through sublimis tendon
transfer for either adduction or opposition.44
Distal Intrinsic Release
Distal intrinsic release may be performed in patients with limited exion of the
PIP joints. A longitudinal incision is made along the dorsal midline of the distal
half of the proximal phalanx. The lateral band and the oblique bers are resected
at the distal third of the proximal phalanx. The severe intrinsic contracture that
involves the meta-carpophalangeal and interphalangeal joints is treated by resection of the lateral tendons of all interossei at the level of the MCP joints. A
temporary arthrodesis by a K-wire through the metacarpophalangeal joint may be
necessary after surgery.
After surgery the hand is splinted with the MCP joints at 180 and the IP joints
activated for free range of motion from the rst postoperative day.42
CONTRACTURE OF THE THUMB CLEFT

The thumb web space includes the soft tissues located between the metacarpals of
the index nger and the thumb. In most cases, contracture of the thumb is associated
with neuromuscular injury of the forearm. The thumb is often involved and has its
own form of intrinsic contracture. Not only contracture of the muscles but also
cicatrization of the skin over the web space and inappropriately applied plaster cast
to immobilize the wrist may cause contracture.
SYMPTOMS
Adduction and exion contracture of the thumb is most disabling. Patients experience problems with gripping and difculties in opposing the ngers because of
the rotated thumb.
CLINICAL FINDINGS
The deformity is characterized by a reduced cleft that separates the thumb and the
ngers. The MCP joint is strongly exed and the interphalangeal joint is hyperextended. The thumb may also be rotated externally and bound rmly to the second
metacarpal. Thereby, the thumb loses its ability to oppose the ngers. The typical
nding may be summarized as a thumb in the palm sign.
TREATMENT
Surgical treatment by excising the fascia and stripping of the contracted muscles
from bones and tenotomies are described.40 The rst interosseous muscle may be
detached from both metacarpals, and the adductors from the thumb may be released
from the third metacarpal. A tendon transfer for opposition of the thumb may be
necessary. In severe cases, excision of the involved muscles in the thumb web may
be required. Tendon transfers and arthrodesis can be performed as indicated.45
125
CONTRACTURE OF FOREARM MUSCLES

SYMPTOMS
Patients with ischemic contracture experience pain, paresthesia, hypoesthesia, and
paresis. They also experience swelling and joint stiffness. The range of motion
amplitude of the wrist joint is decreased, which gives a lack of grip capability.
CLINICAL FINDINGS
In patients with ischemic contracture of the forearm, the wrist is exed, the MCP
joints are hyperextended, and the interphalangeal joints are strongly exed.42
Muscle Tissue
Muscular retraction may be demonstrated by measuring the total passive range of
motion decit. The total decit is the clinical reection of the muscular retraction
in the forearm and in the hand. The summation of values from each of the joints
involved may range from 30 to 200. Muscles become atrophic.
Nerve Tissue
Nerve lesions represent another important feature of the clinical picture. This
includes motor decit of the hand muscles, e.g., contracture of thenar muscles giving
impaired oppositional function. Electromyographic investigation is a valuable aid in
difcult cases. Sensory decits are seldom present without motor involvement. Up
to 60% of patients with motor decit may have normal sensitivity.
Joints
Articular stiffness is difcult to assess initially. The thumb becomes stiff in adduction
and the wrist in exion. Permanent exion of the wrist along with shortening of the
volar ligaments and capsulae are difcult to estimate initially.
Miscellaneous
Dry cyanotic skin and dystrophic nails are common ndings in patients with
ischemic contracture.18
TREATMENT
The goal of the treatment is to regain active and passive range of motion around the
neutral position of the joint. This includes ability of the patient to increase the hand
grip function for common activities of daily living. One should wait at least 3 months
for evidence of spontaneous recovery in the forearm muscles before surgical treatment is initiated.46 Meanwhile, the patient should be treated by physiotherapy,
dynamic orthoses to stimulate function, and static orthoses to adjust malalignment.
Patients with contractures classied as mild or moderate may regain function by
relatively simple procedures.
126
Mild Contractures
Treatment of mild type of contractures within less than a month after injury is a
combination of physical therapy including functional training and dynamic orthosis.
In limited injuries older than one month, dissection or excision of the affected area
is sufcient.20 More extensive mild contractures may need treatment by a muscle
sliding operation. This is performed by releasing the exor muscles from their origin.
In mild cases, tenotomy may sufce.
Moderate Contracture
Patients with moderate contracture may need a muscle-sliding operation, tendon
transfer, or a combination of the two. The muscle-sliding operation is simple and
may be combined with a tendon transfer as a second procedure. One disadvantage
with the muscular release is the decrease in grip strength, particularly in exion of
the distal interphalangeal joint.20 The timing of tendon transfer after excision of
necrotic muscle should be made on the merits of each patient, and depends on the
extent of joint contracture and nerve dysfunction.
Severe Contracture
Patients with severe contractures may improve by different palliative surgical
procedures, such as restoration of nger exion, tenodesis, and arthrodesis. Eichler
and Lipscomb5 preferred an early muscle-sliding operation combined with neurolysis of the median and ulnar nerves as described by Page.47 Early excision of
necrotic muscles and neurolysis may restore sensation and function of the intrinsic
and extensor muscles. Tendon transfer is performed as a secondary procedure after
the injury to the skin and fractures are healed. Patients with severe contractures
may be treated by pedicle graft, tendon transfer, tenodesis, arthrotomy, arthrodesis,
and osteotomy.
Mixed Contractures
In patients with mixed contractures of the hand and forearm, the timing of different
surgical procedures must be regarded.21 Patients must have a good hand sensitivity,
a good passive range of motion in the distal joints, and proximal muscles to stabilize
the arm. It is important to restore an optimal muscle tension during surgery to avoid
postoperative weakness. Muscular activation must provide full nger exion and
extension in any wrist position. The basis for this is to restore the resting sarcomere
length during surgery. The maximum grip strength following this treatment is up to
50% compared with the contralateral side.48
FREE TISSUE TRANSFERS

Encouraging results of treatment by free muscle transfer from one site to another
with complete separation from the donor site has been reported in patients with
ischemic muscular contracture and motor loss in the arm.49
127
Muscle transplantation may be used in patients with signicant functional decit

due to major loss of skeletal muscle. Patients primary functional complaint is lack
of grip capability. These patients have lost all exor muscles but have some remaining
extensor function. The median and ulnar nerves need to be intact. The hand must
have good sensitivity and preserved intrinsic function.48 Other procedures discussed
previously, such as tendon transfers, must have been ruled out before transplantation
is considered.
Free transfer of vascularized skin, nerve, and muscle tissue has shown promising
results. Circulation can be restored to the transplanted muscle by microvascular
anastomosis of the artery and veins of the muscle to suitable vessels in the recipient
site. Transfer of the lateral head of the pectoralis major muscle to the forearm exor
has been suggested.50,51 Free vascularized supercial radial nerve graft to replace
the median nerve has been reported.20,50 Reinnervation by suturing an undamaged
motor nerve in the recipient site to the nerve of the transplanted muscle may result
in muscular contraction activity after 2 to 4 months. Nerve repair and placement of
the muscle at optimum tension are the most important operative steps.48 Patients
may obtain a maximum grip strength that is 50% of normal grip strength.
SUMMARY
Ischemic contracture may be due to an untreated acute compartment syndrome.
Muscle brosis leads to loss of joint motion and imbalance of muscle forces acting
over the joint. It may compress peripheral nerves. Measurements of strength and
range of motion of the whole limb are the most important investigations. The
contracture may be additionally assessed by MRI, sonography, and conventional
radiography. Treatments of contracture include complex soft tissue release, transfer
of muscles and tendons, lengthening of tendons, osteotomy, and arthrodesis.
Entrapped nerves are decompressed early. The goal of treatment is to regain active
and passive range of motion around the neutral position of the joint. This includes
the ability of the patient to stand on plantigrade feet, to use the pinch and grasp
grips of their hands, and to participate in activities of daily living. The aims of
treatment include restitution of nerve function, release of joint contractures, and
replacement of lost muscle function to balance the forces over the joint. The rst
phase is treatment by physiotherapy and supportive and corrective orthoses. In the
second phase, deformities are corrected by surgery of soft tissues. The third phase
includes corrective bone and joint surgery as well as soft tissue releases. The best
time for surgery is when the patient has had peak recovery, usually between 3 and
6 months after the start of contracture.
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31. McCloskey, J.R. and Chung, S.M.K., Quadriceps contracture as a result of multiple
intramuscular injection, Am. J. Dis. Child., 131, 416, 1977.
32. Sasaki, T., Fukuhara, H., Iisaka, H., Monji, J., Kanno, Y., and Yasuda, K., Postoperative evaluation of quadriceps contracture in children: comparison of three different
procedures, J. Pediat. Orthop., 5, 702, 1985.
33. Williams, P.F., Quadriceps contracture, J. Bone Jt. Surg., 50-B, 278, 1968.
34. Jackson, A.M. and Hutton, P.A.N., Injected-induced contractures of the quadriceps
in childhood: a comparison of proximal and distal quadricepsplasty, J. Bone Jt. Surg.,
67-B, 97, 1985.
35. Sengupta, S., Pathogenesis of infantile quadriceps brosis and its correction by
proximal release, J. Pediat. Orthop., 5, 187, 1985.
36. Kasai, M., Operative method and its results for quadriceps muscle contracture, J. Jpn.
Orthop. Assoc., 50, 659, 1976.
37. Iisaka, H., Kato, T., and Sasaki, T., Follow-up study of quadriceps contracture in our
clinic, Hokk. J. Orthop. Surg. Trau. Surg., 20, 33, 1975.
38. Tsubota, K., Doshita, Y., and Imai, T., Contracture of the quadriceps muscle, Orthop.
Surg., 27, 127, 1976.
39. Sacristan, H.D., Sanchez-Barba, A., Stern, L.L.-D., Martin, J.M., Linan, C., and
Ferrandez, L., Fibrosis of the gluteal muscles, J. Bone Jt. Surg., 56-A, 1510, 1974.
40. Bunnell, S., Ischemic contracture, local, in the hand, J. Bone Jt. Surg., 35-A, 88, 1953.
41. Spinner, M., Aliache, A., Silver, L., and Barsky, A.J., Impending ischemic contracture
of the hand: early diagnosis and management, Plast. Reconstr. Surg., 50, 341, 1972.
42. Harris, C. and Riordan, D.C., Intrinsic contracture in the hand and its surgical
treatment, J. Bone Jt. Surg., 36-A, 10, 1954.
43. Littler, J.W., Tendon transfers and arthrodeses in combined median and ulnar nerve
paralysis, J. Bone Jt. Surg., 31-A, 225, 1949.
44. Littler, J.W., The prevention and correction of adduction contracture of the thumb,
Clin. Orthop., 13, 182, 1959.
45. Howard, L.D., Contracture of the thumb, J. Bone Jt. Surg., 32-A, 267, 1950.
46. Seddon, H.J., Volkmanns contracture: treatment by excision of the infarct, J. Bone
Jt. Surg., 38-B, 152, 1956.
47. Page, C.M., An operation for the reief of exion-contracture in the forearm, J. Bone
Jt. Surg., 5-B, 233, 1923.
48. Manktelow, R.T., Zuker, R.M., and McKee, N.H., Functioning free muscle transplantation, J. Hand Surg., 9-A, 32, 1984.
49. Ercetin, . and Akinci, M., Free muscle transfer in Volkmanns ischemic contracture,
Ann. Hand Surg., 13, 5, 1994.
50. Gelberman, R.H. and Botte, M.J., Management of Volkmanns contracture, in Operative Orthopaedics, Chapman, M.W., Ed., Lippincott, Philadelphia, 1988, p. 1131.
51. Ikuta, Y., Kubo, T., and Tsuge, K., Free muscle transplantation by microsurgical
technique to treat severe Volkmanns contracture, Plast. Reconstr. Surg., 58, 407,
1976.
The Crush Syndrome

INTRODUCTION
The term crush injury includes and describes a variety of localized trauma states
associated with injuries to bones and soft tissues. Crush injury is a traumatic injury
severe enough to threaten tissue nutrition and viability. It involves transfer of large
amounts of energy at the accident to the injured tissues.
The term crush syndrome describes the systemic manifestations induced by the
influx of disintegrated products such as myoglobin, potassium, and phosphorus from
muscle necrosis. Patients with major trauma may therefore suffer from two conditions: (1) the local crush injury to the soft tissues, including muscle tissue, and (2)
the secondary systemic effects of destructed muscle tissue, which is labeled crush
syndrome. This chapter focuses mainly on crush syndrome seen in patients with
acute compartment syndrome.
DEFINITIONS
Crush syndrome is defined as the general manifestations of skeletal muscle injury.
Systemic manifestations of the syndrome include hypovolemic shock, electrolyte
derangement, and renal dysfunction. Electrolyte imbalance may even induce cardiac arrhythmia.
Rhabdomyolysis denotes injury to the skeletal muscle cells that liberate their
intracellular contents into the extracellular fluid and the circulation. It may evolve
to a crush syndrome.
HISTORICAL REVIEW
The first reports on rhabdomyolysis appeared in the German literature in 1881.1
Some consequences of crush injury were recognized in the beginning of the 20th
century. They were documented in civilians buried during the 1909 Messina earthquake. Von Colmers in 1909 and Frankenthal in 1916 described muscle necrosis in
soldiers buried under debris as a result of mine explosions.2 Crush injuries were also
described after mining accidents and mob stampedes.
In 1910, Myer-Betz described a syndrome of muscle pain, swelling, and
weakness along with discoloration of the urine.3 Later, it was shown that the
discoloration was caused by myoglobinuria. In 1917, Hackardt first described
anatomic changes of the kidney in patients with muscle necrosis.4 Bywaters and
Beall first used the term crush syndrome in 1941.5 Bywaters estimated that the
crushing injury accounted for about 5% of all casualties during the night raids on
urban areas during World War II.2
131
132
MYOGLOBIN
Myoglobinuria means that myoglobin is present in the urine. Myoglobin is the red
pigment of skeletal muscle and acts as a store of oxygen. The molecule has a weight
of 40,000 Da. It is filtrated in the proximal tubule but cannot be reabsorbed in the
distal tubule, which leads to renal insufficiency due to tubular obstruction. The
molecule is a ferrous protoporphyrin globin complex containing one iron atom per
molecule compared to the four found in hemoglobin. Myoglobin normally comprises
1 to 2% wet weight of skeletal muscle. In highly trained athletes, it may approach
twice as much.
RHABDOMYOLYSIS
Rhabdomyolysis is commonly seen in a variety of clinical conditions such as primary
skeletal muscle disease and systemic diseases that affect skeletal muscle6 and following excessive exertion.7,8 Many cases of rhabdomyolysis, but not all, evolve to
a crush syndrome. Major rhabdomyolysis may be a serious and potentially fatal
condition. It is mainly seen in young men. Exertional rhabdomyolysis has been
reported in physically active individuals. Untrained individuals have larger increase
in postexercise creatine phosphokinase in serum than do trained individuals.9
Patients have muscle soreness, stiffness, and local swelling. Clinical findings
include muscular tenderness and limited range of motion. In laboratory studies, the
concentrations of creatin phosphokinase in serum and myoglobin in urine are elevated. These patients need immediate fluid resuscitation to restore a normal blood
volume and urinary output. Abnormalities of electrolyte concentrations must be
corrected. Diuretics, mannitol, or bicarbonates diuresis may be necessary in severe
cases. Thus, many cases evolve to a crush syndrome.
ETIOLOGY
Muscle injury in patients with crush syndrome may be induced by mechanical forces,
acute traumatic peripheral ischemia, or a combination of both. Pelvic and limb
fractures are commonly associated injuries of the crush syndrome. The syndrome
may be induced by reperfusion following external compression,10,11 overuse of skeletal muscle, heat, alcoholism, viral infections, metabolic disorders, myopathies,
drugs,1214 toxins, and hypokalemia.15 It may occur in patients in knee-chest position
for lumbar spine surgery,16,17 and following urologic surgery in the lithotomy position.11,18 Viral rhabdomyolysis is an acute condition that presents as a viral syndrome
with severe myalgia.6,19 Exertional rhabdomyolysis was diagnosed in patients who
presented with muscle soreness, weakness, and swelling following strenuous physical activity.7,8,2022 It was caused by repetitive exercises in about one half of all
patients with rhabdomyolysis.8
It is important to appreciate whether the muscle is mechanically damaged or
ischemia is the primary cause. This may have a major influence on the choice of
treatment. Most trauma patients with the crush syndrome have some form of massive
external compression for several hours or longer. Knezevich and Torch described a
The Crush Syndrome
133
patient with acute compartment syndrome who developed renal failure and a crush
syndrome in association with streptococcal toxic shock-like syndrome.23
Even if the acute compartment syndrome is treated adequately by decompression, some patients may develop rhabdomyolysis with the crush syndrome and its
systemic manifestations of hypovolemia, acute renal failure, and circulatory insufficiency. Crush syndrome may occur in top athletes with acute compartment syndrome of large muscle groups such as thigh muscles.
PATHOGENESIS
The crush syndrome is caused by leakage of myocyte contents into the circulation.
Disintegration of muscle tissue and the influx of myoglobin, potassium, and
phosphorus into the circulation cause the manifestations. Disintegration of muscle
fibers releases osmotically active particles that promote a fluid shift from the
intravascular space to the interstitial space of a compartment. Each millimole of
osmotically effective particles per kilogram of tissue water exerts a pressure of
19.5 mmHg. This process may create further ischemia and muscle necrosis.
Necrotic muscle from crush injury has 25% of its pigment and phosphorus, ca.
30% of its potassium and creatine, and only 5% of its acid-producing substances
(e.g., glycogen).2
PATHOPHYSIOLOGY
The pathophysiology of the crush syndrome may be based on a model of ischemiareperfusion injury. It may also be due to mechanical forces or external compression,
or both.24 This implies that muscle ischemia induced by arterial and venous obstruction, alterations of capillary permeability, and cellular and interstitial edema may
cause the syndrome.
Reperfusion following prolonged external compression of a limb may lead to
edema formation and abnormally elevated intramuscular pressure, which may induce
secondary ischemia. It has been suggested that most of the damage to the skeletal
muscle fibers occurs during reperfusion rather than during ischemia.2527
The interstitial space is about three times larger than the intravascular space.
Therefore, hypovolemia may develop fast if intravenous substitution is insufficiently
supplied. Massive transudation and extravasation of intravascular fluid initiate hypovolemia, which may lead to hypovolemic shock. Vasoconstriction is unable to compensate for the rapid leakage of plasma, and blood pressure falls.28
Acute renal failure following traumatic injury to skeletal muscle is associated
with hypovolemic shock, impaired renal blood flow, decreased glomerular filtration rate, and intratubular obstruction by myoglobin precipitation and vasoactive quinines from injured skeletal muscle cells that may directly damage the
kidney.29 Therefore, acute renal failure as a result of rhabdomyolysis is more
likely to occur in trained individuals with a large muscle mass, because at trauma
the circulation is exposed to larger quantities of myoglobin and other intracellular
components.
134
Muscle injury
Hypovolemia
Shock
Hyperkalemia
Cardiac arrythmia
Myoglobinemia
Renal failure
FIGURE 9.1 Clinical symptoms induced by muscle injury, which lead to the crush syndrome.
CLINICAL FEATURES
SYMPTOMS
AND
SIGNS
The clinical symptoms include hypovolemic shock, hyperkalemia, and acute renal
dysfunction (Figure 9.1). Patients have dark urine. Even cardiac arrest may occur
after crush injury.30
Skin
Well-localized skin erythema on extremities and buttocks may occur after prolonged
local external compression. Symptoms may start 30 min after release of the external
compression. The injured limb is swollen due to edema, which makes the skin tense
and shiny.
Muscle
The muscles are affected by sudden swelling of the involved limb. Extravasation
of intravascular fluid into the interstitial space may initiate hypovolemia, which
may lead to hypovolemic shock. In nontraumatic cases, patients with rhabdomyolysis experience weakness, myalgia, and tenderness in the affected muscles.
Limb movement may cause severe pain. It may even cause respiratory dysfunction if the diaphragm is involved. Similar symptoms may follow exertional
rhabdomyolysis.31 Muscular rigor is seen in patients whose limbs are compressed
for 10 to 27 h, but not in any patients compressed for 8 h or less.32 Once muscular
rigor is evident, a large fraction of the affected muscle is necrotic. Palpation of
a local induration is diagnostic.
The Crush Syndrome
135
Nerve
Patients generally have lost sensitivity and motor function distal to the injury. Patients
with gluteal compartment syndrome involved often experience sciatic nerve dysfunction.11,33 In most cases, it is impossible to tell whether the muscle, peripheral
nerves, or both are affected.
LABORATORY FINDINGS
Laboratory findings include hyperkalemia, acidosis, hypocalcemia, and hyperphosphatemia released by the damaged muscle fibers. The degrees of creatinine phosphokinase, potassium, and phosphorus levels in serum are good predictors for acute
renal failure in rhabdomyolysis, as well as low serum levels of albumin and the
presence of dehydration.34 Athletic patients with exertional rhabdomyolysis may
have hyperuricemia. Finally, rhabdomyolysis of large muscle groups and associated
capillary endothelial cell dysfunction leak albumin into the interstitial space of the
muscle tissue, leading to hypoalbuminemia. Administration of albumin may increase
the associated interstitial edema.29 Creatine phosphokinase is an enzyme released
by muscles under ischemia or necrosis. Peak serum concentration of creatine kinase
and the number of injured extremities are good estimators of the severity of the
crush syndrome.35 Creatinine phosphokinase levels seen in patients with crush syndrome are much higher than those expected from surgical treatment alone.
CLASSIFICATION
Based on the severity, the syndrome may be classified into three stages.10 Patients
in Stage I have elevated muscle enzymes in serum and myoglobinuria. Patients in
Stage II additionally have oliguria and may be hypotensive. Patients in Stage III
have the full clinical picture of crush syndrome, including shock, oliguria, electrolyte
derangement, and even cardiac arrhythmia.
TREATMENT
Treatment is directed to substitute volume, correct deranged electrolyte balance, and
prevent infection. Rapid institution of forced diuresis and alkalization of the urine
to prevent renal dysfunction are of primary concern. Failure to recognize and to
respond appropriately to the condition may have fatal consequences in up to 25%
of the reports in a literature review11 and in 12% of patients with rhabdomyolysis.6
Adequate cushioning of the patient in the proper position at surgery can prevent
the patient from developing the crush syndrome following prolonged operation. The
lithotomy position with elevated limbs should be interrupted as soon as possible,
especially in elderly patients with impaired peripheral circulation. This position
should not be used more than 2 h.11,36
NONSURGICAL TREATMENT
If multiple large muscle groups are involved in an acute compartment syndrome,
the risk for circulatory hypovolemia and even a hypovolemic shock increases. The
136
initial period of shock is treated by giving adequate volumes of fluid and plasma.
It may be necessary to administer 10 to 12 L of normal saline in the first 12 to
24 h to stabilize the circulation and urine production.29,37 Mannitol may be administered as a single 25-g dose intravenously. Renal failure is the single most
important factor when evaluating the prognosis of the patient with a crush syndrome. Large amounts of myoglobin in the circulation may be filtrated in the
kidneys and occlude the distal tubule, which leads to renal insufficiency. Therefore,
metabolc acidosis should be corrected by adding sodium bicarbonate to alkalize
the urine and increase solubility of myoglobin in the urine. Most authors recommend alkalization of the urine in patients with major rhabdomyolysis whereas
some authors do not.29
Treatment of hypocalcemia per se is not required because it usually corrects
itself spontaneously. Calcium salts may be administered as a means to treat hyperkalemia. Treatment of hyperkalemia is especially important because of its potential
for cardiotoxicity and tendency to induce arrhythmia. Finally, intravenous administrations of glucose and insulin lower the potassium level temporarily.28
In earlier times,infection was a leading cause of death. Currently, the problem
is better controlled by antibiotic therapy combined with incision and drainage of
abscesses, adequate debridement of necrotic liquefied muscle tissue, and treatment
by antibiotics. More than 50% of open fractures are contaminated following treatment by debridement.38
SURGICAL TREATMENT
Successful treatment of acute compartment syndrome by fasciotomy may induce
myoglobinemia. Decompression by fasciotomy may be a prerequisite to diminish
the systemic effects of further muscle necrosis. In most cases, fasciotomy is indicated. Surgical treatment includes debridement, repair of damaged vessels, stabilization of bones, and repair of soft tissues.
Treatment by fasciotomy is controversial if delayed for more than 24 h in patients
with lower-extremity crush injury. These patients suffer increased morbidity and
mortality compared with those treated nonoperatively.32,39 The muscle may bleed
but must not be viable. Reis et al. reported that fasciotomy had no influence on the
survival of muscle, but converted a closed injury into an open one with all the
negative consequences it implies.32
LIQUEFACTION AND CALCIFICATION

Late sequels of untreated leg compartment syndrome are cystic degeneration, liquefaction, and calcification of the soft tissues. Patients present limb deformity following myonecrosis of leg compartments. Cystic degeneration is an uncommon
sequel of acute compartment syndrome. Each of the conditions are defined as a
painless, enlarging mass in a muscle compartment following untreated acute compartment syndrome that presents many years after the trauma. The pathogenesis of
the process is not clear. It has been described in the superficial posterior40 and
anterior41 compartments of the leg.
The Crush Syndrome
137
Plain radiology may reveal a calcific shell. The differential diagnoses are abscess;
malignant tumor; and infection due to parasite, fungi, or mycobacterium infection.
Recommended treatment is excision and primary closure40 or repeated needle
aspiration of the mass.42 Packing the wound and delayed closure may lead to
secondary infection, chronic sinus formation, and limb amputation.
SUMMARY
Crush syndrome is a life-threatening general complication to acute compartment syndrome and other conditions, which causes leakage of myocyte contents into the circulation. Large amounts of hydrogen and potassium ions may be released from the injured
muscle cell and create hyperkalemia, which together with acidosis increase the risks
for cardiac arrhythmia. Clinical symptoms include hypovolemic shock, acute renal
dysfunction, and deranged electrolyte balance (hyperkalemia and abnormally elevated
creatinin phosphokinase levels). This life-threatening condition of the patient is treated
before, during, and after fasciotomy by adequate volume substitution and buffering of
the acidosis. Massive extravasation of fluid may require large volumes of fluid substitution during the first 12 to 24 h of treatment to avoid hypovolemia and oliguria. The
patient needs an indwelling urethral catheter, and the intravenous fluid administration
must ensure a urinary output exceeding 100 mL/h in the adult. If Volkmanns ischemic
contracture is regarded as the local manifestation of an untreated acute compartment
syndrome, the crush syndrome may be regarded as its systemic manifestation.
REFERENCES
1. Fleischer, R., Uber eine neue Form von Haemoglobinurie bein Menschen, Berl. Klin.
Wochenschr., 18, 691, 1881.
2. Bywaters, E.G.L., Ischemic muscle necrosis, J. Am. Med. Assoc., 124, 1103, 1944.
3. Myer-Betz, F., Beobachtungen an einem eigenartigen mit muskellahmungen verbundenen Fall von Hmoglobinurie, Dtsch. Arch. Klin. Med., 101, 85, 1910.
4. Minami, S., Uber Nierenverndrungen nach Verschuttung, Virchows. Arch. f. Path.
Anat., 245, 247, 1923.
5. Bywaters, E.G., and Beall, D., Crush injuries with impairment of renal function., Br.
Med. J., 1, 427, 1941.
6. Gabow, P.A., Kaehny, W.D., and Kelleher, S.P., The spectrum of rhabdomyolysis,
Medicine, 61, 141, 1982.
7. Meyer, R.S. and Mubarak, S.J., Exertional rhabdomyolysis: evaluation and management, Oper. Tech. Sp. Med., 3, 278, 1995.
8. Sinert, R., Kohl, L., Rainone, T., and Scalea, T., Exercise-induced rhabdomyolysis,
Ann. Emerg. Med., 23, 1301, 1994.
9. Hunter, J.B. and Critz, J.B., Effect of training on plasma enzyme levels in man, J.
Appl. Physiol., 31, 20, 1971.
10. Mubarak, S. and Owen, C.A., Compartment syndrome and its relation to the crush
11. Rommel, F.M., Kabler, R.L., and Mowad, J.J., The crush syndrome: a complication
of urological surgery, J. Urol., 135, 809, 1986.
138
12. Kikta, M.J., Meyer, J.P., Bishara, R.A., Goodson, S.F., Schuler, J.J., and Flanigan,
D.P., Crush syndrome due to limb compression, Arch. Surg., 122, 1078, 1987.
13. Klock, J.C. and Sexton, M.J., Rhabdomyolysis and acute myoglobinuric renal failure
following heroin use, W. J. Med., 119, 5, 1973.
14. Owen, C.H., Mubarak, S.J., Hargens, A.R., Garetto, L.P., and Akeson, W.H., Intramuscular pressures with limb compression: clarification of the pathogenesis of druginduced muscle compartment syndrome, N. Engl. J. Med., 300, 1169, 1979.
15. Odeh, M., The role of reperfusion-induced injury in the pathogenesis of the crush
syndrome, N. Engl. J. Med., 324, 1417, 1991.
16. Gordon, B.S. and Newman, W., Lower nephron syndrome following prolonged kneechest position, J. Bone Jt. Surg., 35-A, 764, 1953.
17. Keim, H.S. and Weinstein, J.D., Acute renal failure a complication of spine fusion
in the tuck position: a case report, J. Bone Jt. Surg., 52, 1248, 1970.
18. Reddy, P.K. and Keye, K.W., Deep posterior compartmental syndrome: a serious
complication of the lithotomy position, J. Urol., 132, 144, 1984.
20. Severin, E., Umwandlung des musculus tibialis anterior in Narbengewebe nach beranstrengung, Acta Chir. Scand., 89, 427, 1943.
Bone Jt. Surg., 39-B, 679, 1957.
22. Demos, M.A., Acute exertional rhabdomyolysis, Arch. Int. Med., 133, 233, 1974.
23. Knezevich, S. and Torch, M., Streptococcal toxic shocklike syndrome leading to
bilateral lower extremity compartment syndrome and renal failure, Clin. Orthop.,
254, 247, 1990.
24. Better, O.S. and Stein, J.H., Early management of shock and prophylaxis of acute
renal failure in traumatic rhabdomyolysis, N. Engl. J. Med., 322, 825, 1990.
25. Crinnion, N.J., Homer-Vanniansinkam, S., and Gough, M.J., Skeletal muscle reperfusion injury: pathophysiology and clinical considerations, Cardiovasc. Surg., 1, 317,
1993.
853, 1988.
28. Weeks, R.S., The crush syndrome, Surg. Gyn. Obstet., 127, 369, 1968.
29. Knochel, J.P., Rhabdomyolysis and myoglobinuria, Annu. Rev. Med., 33, 435, 1982.
30. Allister, C., Cardiac arrest after crush injury, BMJ, 287, 531, 1983.
31. Milne, C.J., Rhabdomyolysis, myoglobinuria and exercise, Sp. Med., 6, 93, 1988.
32. Reis, N.D. and Michaelson, M., Crush injury of the lower limbs, J. Bone Jt. Surg.,
68-A, 414, 1986.
Orthop., 132, 57, 1978.
34. Ward, M.M., Factors predictive of acute renal failure in rhabdomyolysis, Arch. Intern.
Med., 148, 1553, 1988.
35. Oda, J., Tanaka, H., Yoshioka, T., Iwai, A., Yamamura, H., Ishikawa, K. et al., Analysis
of 372 patients with crush syndrome caused by the Hanshin-Awaji earthquake, J.
Trau., 42, 470, 1997.
36. Leventhal, I., Schiff, H., and Wulfsohn, M., Rhabdomyolysis and acute renal failure
as a complication of urethral surgery, Urology, 26, 59, 1985.
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139
37. Ron, D., Taitelman, U., Michaelson, M., Bar-Josef, G., Bursztein, S., and Better, O.S.,
Prevention of acute renal failure in traumatic rhabdomyolysis, Arch. Intern. Med.,
144, 277, 1984.
38. Gustilo, R.B. and Anderson, J.T., Prevention of infection in the treatment of one
thousand and twenty-five open fractures of long bones: retrospective and prospective
analyses, J. Bone Jt. Surg., 58-A, 453, 1976.
39. Finkelstein, J.A., Hunter, G.A., and Hu, R.W., Lower limb compartment syndrome:
course after delayed fasciotomy, J. Trau., 40, 342, 1996.
40. Renwick, S.E., Naraghi, F.F., Worrell, R.V., and Spaeth, J., Cystic degeneration and
calcification of muscle: late sequelae of compartment syndrome, J. Orthop. Trau., 8,
440, 1994.
41. Early, J.S., Ricketts, D.S., and Hansen, S.T., Treatment of compartmental liquefaction
as a late sequelae of lower limb compartment syndrome, J. Orthop. Trau., 8, 445,
1994.
42. Malisano, L.P. and Hunter, G.A., Liquefaction and calcification of a chronic compartment syndrome of the lower limb, J. Orthop. Trau., 6, 245, 1992.
10
Etiology and
Pathogenesis of Chronic
INTRODUCTION
Exercise-related muscular pain is seen among athletes and occupational patients who
are exposed to repetitive muscular activity. The painful conditions have been termed
chronic injury, chronic strain, chronic myalgia, repetition strain injury, overuse
injury, and cumulative trauma disorder.1 Up to 15 to 20% of employees are at risk
for developing these conditions. A variety of pathologies on muscle-tendon units
have been suggested. Most patients with muscular diseases have exercise-related
pain and weakness. Symptoms may include anything from benign delayed onset
muscle soreness to exertional rhabdomyolysis.
Chronic leg pain is one of the most common complaints by athletes. Each of
the tissues, including bone, periost, muscle, fascia, tendon, vessels, nerves, and skin,
may elicit pain. These tissues are closely related, especially in the leg and forearm.
It may be difficult to distinguish from which tissue the pain comes. Chronic anterior
compartment syndrome as a cause for anterior leg pain was confirmed only in 10
to 20% of the patients, who were suspected on clinical ground to have the syndrome.2
Possible pathogenetical mechanisms of chronic compartment syndrome may be
classified as (1) increased volume of compartment contents, (2) decreased compliance of the compartment, and (3) external compression or any combination thereof.
HISTORICAL BACKGROUND
The anterior tibial syndrome was first described independently by Severin and
Vogt in 1943.3,4 The anterior tibial syndrome was defined as the triad of (1) necrosis
of the anterior tibial muscle, (2) paralysis of the extensor digitorum brevis muscle,
and (3) anesthesia of the skin over the first interdigital cleft of the foot.5,6 Presently,
anterior tibial syndrome should rather be regarded as an untreated acute compartment syndrome of the anterior compartment of the leg. The terminology march
gangrene was used synonymously with anterior tibial syndrome.7 In a review of
the literature, Bradley in 1973 reported that 33% of all anterior tibial syndromes
were induced by exercise.8 Sixteen percent of these patients had a long history of
recurrent exercise-induced pain in the anterior compartment of the leg predating
the episode.
Carter first suggested a reversible form of anterior tibial syndrome in 1949.5
The chronic, recurrent, reversible form of anterior tibial syndrome was first
141
142
described by Mavor in 1956.9 He described a 24-year-old professional football

player with anterior pain in both legs. The onset coincided with more intensive
training. The patient described the pain as tightness rather than a cramp, and it
forced him to rest. He had no pain at rest after walking or moderate exercise. The
presence of small fascial defects over the anterior compartment indicated the
possibility of increased tension of the fascia due to excessive intramuscular pressure. Mavor treated one patient with chronic anterior compartment syndrome by
incising the fascia over the anterior compartment of the leg. The incision, which
included the fascial gaps, was repaired by a 5 16 cm graft of the fascia lata.9
Others questioned the existence of this syndrome.10,11 However, French and Price
in 1962 and later Reneman in 1968 confirmed the existence of the syndrome by
measurements of intramuscular pressure,12,13 and muscle blood flow.12 To summarize the historical perspectives, the concept of chronic compartment syndrome in
the anterior compartment of the leg is considered to have originated from the
reversible exercise-induced anterior tibial syndrome.
INCREASED VOLUME OF THE COMPARTMENT

Although the etiology of the syndrome is not very well known, the pathogenesis of
the syndrome is fairly well known. Abnormal volume increase of compartment
contents may be caused by exercise, trauma, muscular hypertrophy, venous hypertension, inflammatory changes of muscle tissue, muscle rupture due to repetitive
overloading, or by any combination thereof. Symptoms of the syndrome may also
follow blunt trauma and tumor expansion (Figure 10.1).
Exercise
Trauma
Muscular
hypertrophy
Venous
hypertension
Myocitis
Increased volume of the compartment
Increased intramuscular pressure
Decreased compliance of the compartment
Fascial
thickening
External
compression
Suture of
fascial defect
FIGURE 10.1 Possible reasons for abnormally increased intramuscular pressure in chronic
compartment syndrome.
Etiology and Pathogenesis of Chronic Compartment Syndrome
143
EXERCISE
The symptoms of patients with chronic compartment syndrome are induced by
exercise. Muscle volume may increase up to 20% during maximal normal exercise.
The mode of exercise may influence intramuscular pressure. Intramuscular pressure
at rest is more elevated following eccentric muscular activity compared to concentric
activity.14 Seventy percent of patients with chronic anterior compartment syndrome
are runners.15
Fluid is normally accumulated in exercising muscles.16 The volume of the
anterior compartment increases during exercise.17 The fluid accumulation during
normal exercise increases muscle relaxation pressure during exercise and intramuscular pressure in the anterior tibial muscle at rest after exercise to between 15 and
25 mmHg in normal subjects.1822 In a review of the literature, Bradley8 found that
33% of all acute compartment syndromes were exercise induced. Many of the
patients also had a previous history of exercise-induced leg pain for several years.
In recent decades, this reason for the acute syndrome is less commonly reported,
but the historical view of the problem shows that if the exercise is continued beyond
pain limit in excess, it can develop into the irreversible acute syndrome.
Lawson et al. showed that pressure in the normal asymptomatic anterior
compartment was not significantly different in the anterior compartment of crosscountry skiers using the skating method compared to those using classic skis.23
However, Gertsch et al. presented one patient who developed a chronic anterior
compartment syndrome in the leg after adopting the new cross-country skiing
technique.24 This indicates that the etiology may be complex and probably multifactorial. Beckham et al. measured intramuscular pressure in the anterior compartment after exercise at 80% VO2-max in symptom-free runners and cyclists. Average
pressure in the anterior compartment during VO2-max was 19 mmHg in runners
and 12 mmHg in cyclists. The authors suggested that cycling as a pain-free form
of exercise be tested in patients with chronic anterior compartment syndrome to
determine its efficacy.25 Maximal exercise produced a significant increase of intramuscular pressure in runners as compared to cyclists.25 Endurance running can
induce muscle fiber degeneration in humans.26 However, increased intramuscular
pressure was not responsible for fiber degeneration.27 Hand exercise and exposure
to hand vibration increases intramuscular pressure significantly more in the forearm compared to exercise without vibration in patients.
TRAUMA
Chronic compartment syndrome may follow major trauma to the lower leg28 and
to the forearm.29 Ten percent of patients with chronic anterior compartment
syndrome of the leg had their symptoms following major trauma.30 Even lowvelocity trauma, such as a direct blow injury during a softball game, may precipitate a chronic compartment syndrome.31 In two out of five patients with
chronic compartment syndrome of the lumbar paraspinal muscles, an L1 compression fracture preceded the symptoms of the syndrome.32 The authors speculated that venous stasis or a postthrombotic syndrome, or both, could be contributing etiological factors.
144
MUSCULAR HYPERTROPHY
Muscular hypertrophy as a cause of chronic compartment syndrome has been suggested,
because the syndrome occurs in patients who have a high level of physical activity. The
acute syndrome induced by exercise has been reported in one patient following androgen
therapy.33 Chronic compartment syndrome in the anterior compartment of the leg is not
common among body builders, possibly because they do not exercise these muscles.
Accessory soleus muscles increase intramuscular pressure in the deep posterior compartment but not to the level as that of chronic compartment syndrome.34
VENOUS HYPERTENSION
Deep venous insufficiency may create a volume load of a muscle because the muscle
pump is less effective. Repeated surgery for venous insufficiency has been reported
as an unusual cause of chronic anterior compartment syndrome.28 Plethysmographic
examination showed subnormal values of venous emptying in a few patients with
chronic leg compartment syndrome.35 Patients with incompetent valves of the deep
veins have increased muscle relaxation pressure during exercise but not to the level
as that of chronic compartment syndrome.28 Venous hypertension following thrombosis of the iliac vessels increases intramuscular pressures in both the anterior and
deep posterior compartments.36 Venous hypertension in the leg has also been suggested to follow a Baker cyst or substantial swelling around the knee joint.15 Venous
insufficiency as a cause of chronic compartment syndrome in the lower legs is
probably not common. Severe venous insufficiency was documented in 3% of
patients with chronic anterior compartment syndrome of the leg.37
The anterior tibial muscle is drained by the anterior tibial veins. The veins leave
the anterior compartment through a fascial opening in the proximal part of the
interosseous membrane. If this fascial opening is affected by trauma, it may constitute an anatomical predisposition for compression of the veins. It has been suggested
that the vessels, mainly the veins, may be mechanically compressed between the
herniating muscle tissue and the unyielding fascial edge of an enlarged opening of
the interosseous membrane in chronic compartment syndrome legs (Figure 10.2).
Obstruction of venous flow remains an interesting possible pathogenetic mechanism
for chronic compartment syndrome in the leg.
MYOSITIS
Microtrauma to muscle tissue and excessive stress to the capillary bed and to the
interstitial space of muscle tissue may be explained by the strenuous exercise documented in most chronic compartment syndrome patients. Myositis and inflammatory states in the capillary bed may increase filtration coefficient three- to fivefold.38
This means that increased fluid flow from the capillaries to the interstitial space may
increase the volume and fluid pressure of the space.
OVERLOAD INJURIES
Rupture of few muscle fibers and hemorrhage into the muscle during overexertion
has been described.5 Myofibril change and edema of the fast-twitch fibers follow
145
Muscle
herniation
A.
B.
FIGURE 10.2 (A.) Normal. (B.) Muscle tissue herniation through a fascial defect. Adjacent
vessels may be compressed or pinched between the fascial edge and muscle herniation.
eccentric muscular contractions.14 Intramuscular pressure is elevated after eccentric

muscular activity.14 Other reasons for pain may make muscle relaxation more difficult. High pressure in the tibialis anterior muscle during eccentric muscular contraction is involved in a forceful heel strike.
DECREASED COMPLIANCE OF THE COMPARTMENT

The syndrome most often occurs in locations with relatively unyielding osteofascial
spaces. Increased thickness of the fascia over the anterior compartment was reported
in 25 out of 36 samples.15 In another study, fascial thickness was not increased.37
However, patients in that study had experienced pain for more than 2 years. Therefore, it was difficult to make any conclusions about the fascial thickness at the start
of the syndrome. A mesh-like distension of the fascia covering the muscle is seen
in many patients with chronic anterior compartment syndrome of the leg at surgery.
Sometimes they have multiple small subclinical fascial hernias. Soffer et al. reported
one patient with an aberrant fascial band overlying and tightly compressing the fascia
over the anterior compartment of the leg.39
Suturing of fascial defects is never indicated. Decreased volume of the compartment following suture may increase intramuscular pressure and elicit an acute
compartment syndrome.40
External compression increases intramuscular pressure at rest and muscle relaxation
pressure during exercise. Muscle relaxation pressure is the pressure in the muscle
between contractions (Figure 10.3). External compression by tight stockings and
braces may increase muscle relaxation pressure during exercise.41,42 Volume of the
compartment is not increased; rather, it may be decreased. The local blood perfusion
146
Pressure
A.
B.
Time
FIGURE 10.3 Redrawing from an original intramuscular pressure recording during concentric muscular activity. Pressure recording without (A) and with (B) external compression, e.g.,
a knee brace. During external compression of the leg (after arrow), the muscle relaxation
pressure that occurs between contractions is elevated. The time period for muscle relaxation
pressure is indicated by the bars.
pressure decreases by increased muscle relaxation pressure and intramuscular pressure at rest after exercise. Patients with elevated intramuscular pressure experience
premature muscle fatigue. In another study, pressures were recorded in the leg and
thigh without a knee brace and with a brace applied with strap tensile force of 25 N,
50 N, and a force preferred by the subject. External compression caused by the brace
increased intramuscular pressure at rest and muscle relaxation pressure during exercise three- to tenfold compared to normal pressure.43 The pressure increased to
between 30 and 54 mmHg. Local blood perfusion pressure in the supine subject
decreased up to 42%.43 In other studies, these pressure levels have been shown to
decrease local muscle blood flow and induce premature muscle fatigue.4447 Pressures
increased relatively more in the braced leg compared to the braced thigh. This is,
of course, not a chronic compartment syndrome, although symptoms and metabolic
changes may be similar. External compression of a limb may induce relative
ischemia. Following ischemia, endothelial cells may leak abnormal volumes of
plasma or water into the interstitial space of the muscle and induce abnormally
elevated intramuscular pressure. Eiken and Bjurstedt found that exercise performance was reduced by 40% due to muscle fatigue in subjects who were exposed to
a supraatmospheric pressure of 50 mmHg.48
SUMMARY
Possible pathogenetic mechanisms include increased volume, decreased compliance, and external compression of the compartment. Abnormal volume increase
of the compartment contents may be caused by exercise, trauma, muscular
hypertrophy, venous hypertension, inflammatory changes of muscle tissue, and
muscle rupture due to repetitive overloading. Suturing of fascial defects is never
indicated. Decreased volume of the compartment may increase intramuscular
147
pressure and elicit an acute compartment syndrome. External compression

caused by orthotic applications may increase intramuscular pressure at rest and
muscle relaxation pressure during exercise to levels that elicit premature muscle
fatigue caused by ischemia. The most common reason for chronic compartment
syndrome in the leg is increased volume of the anterior compartment, which
increases the muscle relaxation pressure during exercise and intramuscular pressure at rest after exercise.
REFERENCES
1. Fleckenstein, J.L. and Shellock, F.G., Exertional muscle injuries: magnetic resonance
imaging evaluation, Tech. Orthop., 7, 50, 1992.
2. Styf, J., Diagnosis of exercise-induced pain in the anterior aspect of the lower leg,
Am. J. Sp. Med., 16, 165, 1988.
3. Severin, E., Umwandlung des musculus tibialis anterior in Narbengewebe nach
beranstrengung, Acta Chir. Scand., 89, 427, 1943.
4. Vogt, P.R., Ischemic muscular necrosis following marching, read before the Oregon
State Medical Society, 1943 (cited by Horn, 1945).
Lancet, 19, 928, 1949.
Bone Jt. Surg., 39-B, 679, 1957.
7. Sirbu, C.A.B., Murphy, M.J., and White, A.S., Soft tissue complications of fractures
of the leg, West. Med., 60, 53, 1944.
289, 1973.
9. Mavor, G.E., The anterior tibial syndrome, J. Bone Jt. Surg., 38-B, 513, 1956.
10. Griffiths, D.L., The anterior tibial syndrome: a chronic form, J. Bone Jt. Surg., 38 B,
438, 1956.
11. Grunwald, A. and Silberman, Z., Anterior tibial syndrome, JAMA, 171, 132, 1959.
12. French, E.B. and Price, W.H., Anterior tibial pain, Brit. Med. J., 6, 1290, 1962.
Thesis, University of The Hague, 27, 1968.
14. Fridn, J., Sfakianos, P.N., Hargens, A.R., and Akeson, W.H., Residual muscular
swelling after repetitive eccentric contractions, J. Orthop. Res., 6, 493, 1988.
15. Detmer, D.E., Sharpe, K., Sufit, R.L., and Girdley, F.M., Chronic compartment syndrome: diagnosis, management and outcomes, Am. J. Sp. Med., 13, 162, 1985.
16. Jacobsson, S. and Kjellmer, I., Accumulation of fluid in exercising skeletal muscle,
17. Gershuni, D.H., Gosink, B.B., Hargens, A.R., Gould, R.N., Forsythe, J.R., Mubarak,
S.J. et al., Ultrasound evaluation of the anterior musculofascial compartment of the
leg following exercise, Clin. Orthop., 167, 185, 1982.
18. Crenshaw, A., Styf, J., and Hargens, A., Intramuscular pressures during exercise: an
evaluation of a fiber transducer-tipped catheter system, Eur. J. Appl. Physiol., 65,
178, 1992.
19. Rosfors, S., Eriksson, M., and Akermark, C., Intramuscular pressure recording in the
assessment of patients with suspected chronic compartment syndrome, Scand. J. Med.
Sci. Sp., 3, 52, 1992.
148
20. Styf, J.R. and Krner, L.M., Microcapillary infusion technique for measurement of
intramuscular pressure during exercise, Clin. Orthop. Rel. Res., 207, 253, 1986.
21. Styf, J., Forsblad, P., and Lundborg, G., Chronic compartment syndrome in the first
dorsal interosseous muscle, J. Hand Surg., 12A, 757, 1987.
22. Styf, J.R., Intramuscular pressure measurements during exercise, Oper. Tech. Sp.
Med., 3, 243, 1995.
23. Lawson, S.K., Reid, D.C. and Wiley, J.P., Anterior compartment pressures in crosscountry skiers, Am. J. Sp. Med., 20, 750, 1992.
24. Gertsch, P., Borgeat, A., and Wlli, T., New cross-country skiing technique and
compartment syndrome, Am. J. Sp. Med., 15, 612, 1987.
25. Beckham, S.G., Grana, W.A., Buckley, P., Breazile, J.E., and Claypool, P.L., A
comparison of anterior compartment pressures in competitive runners and cyclists,
Am. J. Sp. Med., 21, 36, 1993.
26. Warhol, M.J., Siegel, A.J., Evans, W.J., and Silverman, L.M., Skeletal muscle injury
and repair in marathon runners after competition, Am. J. Pathol., 118, 331, 1985.
27. Binkhorst, F.M.P., Slaaf, D.W., Kuipers, H., Tangelder, G.J., and Reneman, R.S.,
Exercise-induced swelling of rat soleus muscle: its relationship with intramuscular
pressure, J. Appl. Physiol., 69, 67, 1990.
28. Styf, J., Chronic anterior compartment syndrome of the lower leg, Ph.D. Thesis,
University of Gteberg, 174, 1986.
29. Kutz, J.E., Singer, R., and Lindsay, M., Chronic exertional compartment syndrome
of the forearm: a case report, J. Hand Surg., 10, 302, 1985.
30. Styf, J.R. and Krner, L.M., Diagnosis of chronic anterior compartment syndrome
in the lower leg, Acta Orthop. Scand., 58, 139, 1987.
31. Creighton, C., Tubb, M.C., and Vermillion, D., Chronic exertional compartment
syndrome after minor injury to the lower extremity, Milit. Med., 166, 366, 2001.
Spine, 12, 680, 1987.
33. Halpern, A.A. and Nagel, D.A., Bilateral compartment syndrome associated with
androgen therapy, Clin. Orthop., 128, 243, 1977.
34. Melberg, P.E. and Styf, J., Posteriomedial pain in the lower leg, Am. J. Sp. Med., 17,
747, 1989.
35. Qvarfordt, P., Christenson, J.T., Eklf, B., Ohlin, P., and Saltin, B., Intramuscular
pressure muscle blood flow and skeletal muscle metabolism in chronic anterior tibial
compartment syndrome, Clin. Orthop. Rel. Res., 179, 284, 1983.
Surgery, 95, 191, 1984.
37. Turnipseed, W., Detmer, D.E., and Girdley, F., Chronic compartment syndrome, Ann.
Surg., 210, 557, 1989.
Scand., 104, 318, 1978.
39. Soffer, S.R., Martin, D.F., Stanish, W.D., and Michael, R.H., Chronic compartment
syndrome caused by aberrant fascia in an aerobic walker, Med. Sci. Sp. Exerc., 23,
304, 1991.
40. Mubarak, S.J., Surgical management of chronic compartment syndromes of the leg,
Oper. Tech. Sp. Med., 3, 259, 1995.
149
41. Styf, J., Nakhostine, M., and Gershuni, D., Functional knee braces increase intramuscular pressures in the anterior compartment of the leg, Am. J Sp. Med., 20, 46,
1992.
42. Styf, J., Lundin, O., Petras, S., and Gershuni, D., Prophylactic knee braces impair
local muscle function, Am. J. Sp. Med., 22, 830, 1994.
43. Lundin, O. and Styf, J.R., Intramuscular pressure in the leg and thigh related to tensile
strap forcee during knee brace wear, Am. J. Sp. Med., 26, 567, 1998.
44. Ashton, H., The effect of increased tissue pressure on blood flow, Clin. Orthop. Rel.
Res., 113, 15, 1975.
45. Ogata, K. and Whiteside, L.A., Effects of external compression on blood flow to
muscle and skin, Clin. Orthop., 168, 105, 1982.
blood flow disturbances produced by simultaneously elevated venous and total muscle
48. Eiken, O. and Bjurstedt, H., Dynamic exercise in man as influenced by experimental
restriction of blood flow in the working muscles, Acta Physiol. Scand., 131, 339, 1987.
11
Pathophysiology of
Chronic Compartment
Syndrome
INTRODUCTION
The pathophysiology of chronic compartment syndrome describes how abnormally

increased intramuscular pressure in a compartment affects muscle blood ow, tissue
oxygenation, and neuromuscular function.13 It also includes the study of how
patients are affected by local muscular ischemia4,5 and exercise-induced pain. Basic
understanding of the pathophysiology of chronic compartment syndrome enhances
the ability to diagnose this syndrome by clinical means as well as the understanding
of other conditions of chronic leg pain.
SWELLING
OF
MUSCLE TISSUE
DURING
EXERCISE
Muscle tissue normally swells during exercise. The swelling is most pronounced in
the interstitial space. Swelling per unit area of the interstitial space is twofold higher
than muscle ber swelling per unit area.6 In animal experiments, it has been shown
that the lymph ow can probably drain the entire protein content of the capillary
ltrate produced during exercise.7 The increased volume of skeletal muscle during
exercise is due to increased regional muscle blood ow and transcapillary ltration
into the interstitial space. Data from human studies indicate that muscle blood ow
during exercise is between 50 and 100 mL/min/100 g,8 although values of up to 200
mL/min/100 g have been reported.8,9 The mechanical inuence of muscle contractions on ow rate is reasonable explanation for the higher muscle blood ows in
conscious animals during exercise.8 The amount of capillary ltrate accumulating
in exercising muscle depends on the workload. The most important limiting factor
for ltration into the interstitial space is the increased interstitial hydrostatic pressure.10 Transcapillary uid loss into leg muscles during heavy exercise during 6 min
is 45 mL/kg.11 After 15 min of work, the total amount of uid accumulation averages
14.8 mL/100 g tissue.12
The compliance of the interstitial space in skeletal muscle is high at rest,13 when
intramuscular pressure is within the normal range. Substantial amounts of uid can
be mobilized from or added to the interstitial space of skeletal muscle with only
small alterations of the tissue uid pressure (Figure 15.9). Most authors believe that
the symptoms and the dysfunction elicited by the syndrome are due to ischemia
whereas others believe they are not related to ischemia.14
151
152
REGULATION OF LOCAL MUSCLE BLOOD FLOW

Theories on muscle blood ow at rest are discussed in Chapter 4. In the present
chapter, these theories are applied for conditions with exercising muscles. The effects
of increased muscle relaxation pressure during exercise, i.e., the pressure between
contractions, on local perfusion pressure and muscle blood ow are discussed.
Results from clinical studies are compared with theories on microvascular occlusion
and critical closing pressure.
PERFUSION PRESSURE (PP)

The arteriovenous gradient theory is based on the hydrodynamic principles described
in the Law of Poiseuille:
Q = k(P1 P2) r4/L n
(11.1)
According to this law, uid ow (Q) is directly proportional to the pressure difference
(P1 P2) over the tubing or vessel and to the fourth dimension of the radius (r).
Fluid ow is indirectly proportional to the length of the vessel (L) and to the viscosity
of the uid (n). The constant k = p/8. In Equation 11.2, the resistance (R) is directly
proportional to the length of the vessel and the uid viscosity (n):
R = 8L n/p r4
(11.2)
Therefore, if Equation 11.1 is combined with Equation 11.2, muscle blood ow

(MBF) by the arteriovenous gradient theory can be expressed as:
MBF = (Pa Pv)/R
(11.3)
The perfusion pressure (PP) is the difference between the pressure at the arterial
(Pa) and the venous (Pv) end of the capillary (Figure 11.1). Pa may be expressed
as mean arterial pressure (MAP). Pressure inside patent veins (Pv) can never be less
than the extramural pressure,15 which is the total tissue pressure in the interstitial
space. Therefore, muscle relaxation pressure (MRP) during exercise and intramuscular pressure at rest after exercise are equal to Pv in Equation 11.3. The local PP
during muscle relaxation may therefore be expressed as:
PP = MAP MRP
(11.4)
MRP in Equation 11.4 may be replaced with intramuscular pressure at rest after
exercise. Increased intramuscular pressure reduces the local arteriovenous pressure
gradient, and thereby reduces the local MBF.3,16,17
MICROVASCULAR OCCLUSION
Normal capillary pressure at rest is between 20 and 30 mmHg. The limiting factor
in the MBF disturbances has been shown to be at the capillary level.18,19 Increased
Pathophysiology of Chronic Compartment Syndrome
153
Pressure
MAP
MAP
Perfusion pressure
Pv
Pv
Abnormally increased
muscle relaxation pressure
Muscle relaxation pressure

A. Normal MRP
B. Elevated MRP
FIGURE 11.1 Perfusion pressure in a subject with normal muscle relaxation pressure (A)
and a patient with chronic compartment syndrome (B). MAP is the mean arterial pressure
and Pv is the intravenous pressure. Perfusion pressure is signicantly lower in patients with
chronic compartment syndrome due to the increasing muscle relaxation pressure during
exercise.
intramuscular pressure causes capillary vessels to collapse at their distal end.20 It

has been shown that increased MRP values to between 35 and 55 mmHg in chronic
compartment syndrome patients impair local MBF and elicit the clinical symptoms
of the syndrome.3 These ndings may be explained by both the arteriovenous
gradient theory and the theory of microvascular occlusion.
CRITICAL CLOSING PRESSURE

The critical closing pressure theory postulates that a vascular bed may be exposed
to zero blood ow in the presence of a positive PP. Perfusion pressure is dened as
the difference between mean artery pressure and the intramuscular pressure. The
pathogenetical mechanism for vascular collapse in the presence of a positive transmural pressure may alter with vasomotor tone. The transmural arteriolar pressure at
which blood ow ceases is an index of critical closing pressure. The physiological
event has also been described as ow cessation pressure.21 Evidence for this concept
was reported by Ashton,21 who showed that the positive pressure intercept at zero
ow was 33.4 (range 10 to 68) mmHg in the forearm of normal subjects at rest.
This nding was explained as active closure of the small arteries in muscle tissue.22
The work of Roddie and Shepherd also supported the concept of critical closing
pressure, but they found no signs of arteriolar constriction in response to a rise in
venous pressure.23
With this theory, it is possible to explain how patients with chronic compartment syndrome have decreased local MBF in the presence of positive PP. The
critical opening transmural pressure was 5 to 10 mmHg higher than the closing
pressure.24 This implies that once the vasculature closed, it was more difcult to
154
open. This nding was also observed by Chang et al., who reported a signicant
difference of critical opening and critical closing pressure of the vasculature during
external compression.25
TIDAL WAVE THEORY

Dahn et al.26 found that MBF did not cease until intramuscular pressure reached the
systolic blood pressure when venous stasis was used. They also found that MBF stopped
when the locally applied external pressure was equal to the diastolic blood pressure at
rest. The explanation for this is given by the tidal wave theory, or Starling valve theory,
which postulates that the microcirculation does not remain open long enough to allow
for pulsatile muscle blood ow. They concluded that the diastolic blood pressure, rather
than the MAP, determined the driving pressure over the vasculature.
The contraction frequency, level of muscle pressure during contractions, and
the time period for muscle relaxation between contractions are important to control
during exercise studies. If contraction frequency is high and time period for muscle
relaxation short enough, the microcirculation may not stay open long enough to
allow for pulsatile MBF. Rodbard and Pragay found by comparing the effects of
various muscular contractions that the number of contractions increased with the
muscle relaxation time.27
MUSCLE BLOOD FLOW IN CHRONIC

COMPARTMENT SYNDROME
Skeletal muscle is not perfused during contraction,28 and arterial inow to the muscle
vascular bed occurs only between contractions.29,30 For these reasons, MRP during
exercise, i.e., the pressure between contractions, is an important pressure parameter to
study.3,31,32 MRP exceeding 35 mmHg during exercise impedes MBF and is well
correlated with the development of swelling, pain, and impaired function of the tissues
within the compartment.3,32 The symptoms of the syndrome correlate well with the
decreased local PP, which is the calculated difference between mean arterial blood
pressure and MRP during exercise as described in Equation 11.4.31,32 These patients
have normal MBF values in the beginning of exercise (Figure 11.2). MBF decreases
signicantly at the end of exercise.3 In another study, patients with elevated intramuscular pressure during exercise had impaired MBF.33 Other animal and human studies
on the inuence of increased intramuscular pressure at rest on MBF have demonstrated
a signicant decrease or even cessational ow when tissue pressure exceeds 30 to 60
mmHg.18,22,34,35 These results concur with the different theories on the mechanisms of
how increased intramuscular pressure affects MBF. They also concur on factual measurements in patients with chronic anterior compartment syndrome in the leg.3
Reneman et al. showed that a combined increase in venous and total intramuscular pressure resulted in cessation of muscle capillary blood ow in the presence
of arteriolar dilatation.19 They concluded that the arterioles were not the limiting
factor in MBF disturbances in simulated compartment syndromes. They found that
muscle capillary blood ow stopped while there was a positive transmural pressure
of 24 mmHg over the vascular bed.
155
MBF (mL/100g/min.)
70
60
50
40
30
20
10
MRP/IMP
10
20
30
40
50
60 mmHg
FIGURE 11.2 Correlation diagram of individual values of muscle blood ow (MBF) and
muscle relaxation pressure (MRP) in patients with chronic compartment syndrome before
surgery. Dots indicate results after 3 min of exercise without pain in the leg. Circles indicate
results at the end of exercise when the leg is painful and muscle function is impaired. The
bars indicate one standard deviation. (Redrawn from Styf, J., Suurkula, M., and Krner, L.,
J. Bone Jt. Surg., 69-B, 301, 1987.)
NEUROMUSCULAR FUNCTION IN CHRONIC

Patients with chronic compartment syndrome develop muscular weakness during
exercise (Figure 11.3). Pain and ischemia may impair torque generation of the
muscles involved. Skeletal muscle is sensitive to pressure and direct trauma. Nerve
endings are located in the walls of the blood vessels. Ischemia may induce premature
muscle fatigue. Muscle bers themselves are probably insensitive to painful stimuli.
However, pain may induce muscle weakness due to inhibition of muscular function.
Only in a few patients is there sensory dysfunction at clinical investigation following
an exercise test.36
MUSCULAR OXYGENATION IN CHRONIC

Previous studies have demonstrated decreased MBF as well as impaired muscle
oxygenation.4 These ndings suggest ischemia as etiology for chronic compartment
syndrome. Changes in intramuscular oxygenation may be measured by a continuous
dual wavelength near-infrared spectrometer. The device measures reection of light
transmitted at wavelengths of 760 and 850 nm. Deoxygenated hemoglobin absorbs
156
Abnormally increased muscle relaxation pressure
Decreased local
muscle blood flow
Decreased tissue
oxygenation
Decreased nerve
conduction velocity
Ischemia
Impaired muscle function
FIGURE 11.3 Pathophysiology of chronic compartment syndrome is based on abnormally

elevated muscle relaxation pressure during exercise.
more light at 760 nm, whereas oxygenated hemoglobin absorbs more light at 850 nm.
Myoglobin has absorption characteristics identical to those of hemoglobin.
Impaired muscle oxygenation has been demonstrated in human experimental
models on chronic compartment syndrome37,38 as well as in patients with chronic
anterior compartment syndrome in the leg.4,5 Diagnosis of chronic compartment
syndrome by near-infrared spectroscopy is based on a slow reoxygenation and default
reactive hyperemia (Figure 11.4).
Contractions of an ischemic skeletal muscle bed induce pain and impaired
muscle function. Clinical examples of this are patients with chronic compartment
syndromes and intermittent claudication. Therefore, muscle contractions appear to
be necessary for development of pain in chronic compartment syndrome.
SUMMARY
All muscles swell during exercise. The increased volume of skeletal muscle during
exercise is due to increased blood ow and transcapillary ltration into the interstitial
space of the muscle. Arterial inow to the working muscle occurs between contraction, i.e., during muscle relaxation. Abnormally increased MRP during exercise
affects local MBF and induces ischemia and pain during exercise. Intramuscular
pressure at rest after exercise does not normalize within 10 min. Changes of intramuscular oxygenation during exercise and at rest after exercise may be measured
by near-infrared spectroscopy. Changes of local MBF may be measured at rest after
exercise by photopletysmography.
157
1 min.
Tissue oxygenation
Time
FIGURE 11.4 Tissue oxygenation measured by near-infrared spectroscopy. The bold line
shows the changes in a normal subject. Patients with chronic compartment syndrome (dotted
line) have delayed recovery of tissue oxygenation. The time bar indicates the time period of
concentric exercise.
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20. Beer, G., Role of tissue uid in blood ow regulation, Circ. Res., 28/29 (Suppl. 1),
154, 1971.
21. Ashton, H., Critical closing pressure in human peripheral vascular bed, Clin. Sci.,
22, 79, 1962.
22. Ashton, H., The effect of increased tissue pressure on blood ow, Clin. Orthop. Rel.
Res., 113, 15, 1975.
23. Roddie, I.C. and Shepherd, J.T., Evidence for critical closure of digital resistance
vessels with reduced transmural pressure and passive dilatation with increased venous
pressure, J. Physiol., 136, 498, 1957.
24. Ashton, H., Reopening of blood vessels after critical closure, Clin. Sci., 22, 95, 1962.
25. Chang, D.S., Breit, G.A., Styf, J.R., and Hargens, A.R., Cutaneous microvascular
ow in the foot during simulated variable gravities, Am. J. Physiol., 271, R961, 1996.
26. Dahn, I., Lassen, N.A., and Westling, H., Blood ow in human muscles during
external pressure or venous stasis, Clin Sci, 32, 467, 1967.
27. Rodbard, S. and Pragay, E.B., Contraction frequency blood supply and muscle pain,
J. Appl. Physiol., 24, 142, 1968.
28. Barcroft, H. and Millen, J.L.E., The blood ow through muscle during sustained
contraction, J. Physiol., 97, 17, 1939.
29. Folkow, B., Gaskell, P., and Waaler, B.A., Blood ow through limb muscles during
heavy rhytmic exercise, Acta Physiol. Scand., 80, 61, 1970.
30. Mortimer, J.T., Kerstein, M.D., Magnusson, R., and Petersen, I., Muscle blood ow
in the human biceps as a function of developed muscle force, Arch. Surg., 103, 376,
1971.
159
pressure muscle blood ow and skeletal muscle metabolism in chronic anterior tibial
34. Clayton, J.M., Hayes, A.C., and Barnes, R.W., Tissue pressure and perfusion in the
compartment syndrome, J. Surg. Res., 22, 333, 1977.
35. Sheridan, G.W. and Matsen, F.A., An animal model of the compartmental syndrome,
Clin. Orthop., 113, 36, 1975.
Am. J. Sp. Med., 16, 165, 1988.
1979.
12
Clinical Diagnosis of
Chronic Compartment
Syndromes
INTRODUCTION
Chronic compartment syndrome is defined as a painful condition in which increased

intramuscular pressure during exercise impedes muscle blood flow and impairs
function of the tissues within the compartment.1,2 Diagnosing the causes of chronic
pain induced by exercise in the extremities is difficult because patients have few or
no specific symptoms at rest. Depending on location and severity of symptoms,
exercise tests may include concentric muscular activity against resistance (e.g., body
weight), indoor walking, exercise on an ergometer, running on a treadmill, or outdoor
running on a track or field. Upper-extremity exercise may include whipping with a
whisk, playing a musical instrument, throwing a ball repeatedly, pulling the reins
tight during simulated harness racing, or any activity that elicits the symptoms. A
work simulator is most helpful.3,4 The important thing is to induce the patients
effort-related symptoms and signs by an exercise test and to perform a clinical
examination when the patient is symptomatic or in pain.
SYMPTOMS AND CLINICAL FINDINGS

Symptoms and clinical findings correlate well with the pathophysiology (Figure
12.1). Patients complain of local swelling, tightness, and pain during and at rest
after physical activity.1,2,58 Swelling is a sign of increased volume of the compartment. Fascial defects may be related to the increased tension created by the increased
volume of the compartment contents. Muscle tissue may herniate through the fascial
defects. The ischemic muscle pain is intense enough to force the athlete to stop the
activity. The symptoms reverse within 20 min to hours at rest. Sometimes patients
describe clumsiness and weakness at the time of pain. The athletes experience
ischemic pain that force them to quit exercising when blood flow decreases.2,6,9,10
At clinical investigation, the compartment muscles are hard on palpation following exercise. The impaired muscle function at the end of an exercise test can be
evaluated clinically by estimating the strength of an active contraction against resistance. Decreased force generation in this situation is a sign of impaired muscle
function induced by ischemia and pain (Figure 12.1). Nerve dysfunction impairs
sensitivity and also induces muscular weakness. Dysesthesia may be recorded in a
few cases.9,11 Distal pulses are always normal.
161
162
Pathophysiology
Symptoms
Exercise
Swelling
Fascial defects
Increased volume
Muscle herniation
Increased pressure
Decreased muscle
blood flow
Premature muscle fatigue

Pain
Ischemia
Weakness
Sensory dysfunction
FIGURE 12.1 The connection between pathophysiology and symptoms in chronic compartment syndrome.
CHRONIC ANTERIOR COMPARTMENT

SYNDROME IN THE LEG
A patients history of pain induced only during exercise, occurring only in the
anterior aspect of the leg, and requiring the patient to interrupt the physical activity
suggests chronic anterior compartment syndrome. Between 70 and 80% of patients
who were operated on for the syndrome in the leg were runners.6,9,12 The syndrome
is bilateral in 60 to 90% of the patients.1,9,13 A patients pain drawing is a helpful
tool to investigate single and multiple locations, as well as impaired sensation distal
to the affected compartment (Figure 12.2). Table 12.1 compares the history of a
group of patients with chronic anterior compartment syndrome in the leg and patients
with chronic anterior leg pain for other reasons.
SYMPTOMS
Most patients are symptom-free at rest. Pain with multiple locations in the leg
induced by a short running distance, and allowing the patient to continue running
despite the pain, indicates an etiology of noncompartment syndrome.6 Clinical investigation following an exercise test that elicits the symptoms is particularly useful.
Swelling is a sign of increased volume of the compartment. Following an exercise
test, patients experience pain over the muscles of the anterior compartment.
Clinical Diagnosis of Chronic Compartment Syndromes
I.
163
II.
FIGURE 12.2 Two examples (I and II) of pain drawings by patients with chronic anterior
leg compartment syndrome.
SIGNS
Between 30 and 50% of patients with the syndrome are tender at palpation over the
anterior margin of the tibia. These patients have periostitis of the anterior margin of
the tibia.6,10 Muscle herniation is seen in 20 to 60% of patients.14 Decreased sensitivity over the first interdigital cleft and the dorsum of the foot is a sign of impaired
nerve function,9,11 which sometimes occurs in patients with chronic anterior compartment syndrome. However, few patients report these symptoms spontaneously.
Recordings of nerve conduction velocity and the EMG signal are both usually normal
when recorded at rest.1,9 The impaired muscle function at the end of an exercise test
can be evaluated clinically by testing the strength of active dorsiflexion against
manual resistance. MRI and phlebography are not useful in diagnosis of compartment syndrome. However, near-infrared spectroscopy,15 laser Doppler flowmetry,16
and thallium-201 chloride scintigraphy17,18 have been suggested as useful tools to
diagnose the syndrome.
In summary, a patients history indicates chronic anterior compartment syndrome if pain is induced only by athletic activity, pain that occurs only in the anterior
aspect of the leg, and pain that forces the athlete to interrupt running.6 A patients
history does not indicate chronic anterior compartment syndrome if there is pain
with multiple locations in the leg or if pain is induced by a short running distance,
allowing the athlete to continue running despite the pain (Table 12.1).
CHRONIC LATERAL COMPARTMENT SYNDROME

IN THE LEG
Only a few cases of chronic lateral compartment syndrome have been published.1,6,10,19 It has been seen to occur in 10%1 and in less than 5%9 of patients
with chronic anterior compartment syndrome. It has been suggested that history
164
TABLE 12.1
Results of History by a Questionnaire and Clinical Findings at Rest
Before Physical Exercise in 80 Patients with Suspected Chronic
Anterior Compartment Syndrome (CACS) who were Referred to
an Orthopedic Clinica
History
Only anterior location of leg pain
Pain induced only by running
Pain necessitating interruption of running
Pain only at rest after running
Pain during walking
Running distance that induced pain (km)
Range of running distance (km)
CACS
(n = 22)b
non-CACS
(n = 58)b
68%
55%
55%
0%
27%
4.5
0.210
29%
10%
12%
12%
29%
0.6
0.013
Clinical Findings at Rest Before Exercise

No tenderness over the anterior margin
55%
Tenderness only over the anterior margin
32%
Tenderness over other locations in the leg
14%
Tenderness over the anterior tibial muscle
18%
Muscle hernia over the anterior compartment
23%
Muscle hernia over the lateral compartment
0%
Pes cavus or pes pronatus
14%
24%
19%
76%
17%
3%
5%
14%
Following diagnosis by intramuscular pressure recordings during exercise and at rest

after exercise, 22 patients with CACS in the leg are compared with 58 patients with
chronic anterior pain (non-CACS) for other reasons.
b Number of patients.
Source: From Styf, J.R. and Krner, L.M., Acta Orthop. Scand., 58, 139, 1987.
is often sufficient to establish the diagnosis.1 However, in a study of 22 patients

with anterolateral pain, only 1 proved to have the syndrome in the lateral
compartment as verified by intramuscular pressure recordings.9,20 As reflected
by the literature, the syndrome seems to be an unusual cause of pain in the
lateral compartment. The peroneus tunnel syndrome has been reported to be a
more common reason for anterolateral pain than chronic lateral compartment
syndrome has.9,20,21 The differential diagnosis of anterolateral leg pain is discussed in Chapter 14.
SYMPTOMS
The pain is located over the lateral compartment. Patients may experience
pricking sensation or numbness over the ankle joint and dorsum of the foot after
an exercise test.
I.
165
II.
FIGURE 12.3 Pain drawings by two patients with chronic lateral compartment syndrome in
the leg.
SIGNS
Most patients have a fascial defect and muscle herniation 10 to 12 cm proximal of
the lateral malleolus. Sensitivity may be disturbed over the dorsum of the foot. The
sensitivity over the first interdigital cleft is normal (Figure 12.3).
CHRONIC POSTERIOR COMPARTMENT SYNDROME

IN THE LEG
The existence of a chronic compartment syndrome in the deep and superficial
posterior compartments is a controversial topic. Posteromedial leg pain, which is
clinically diagnosed as medial tibial syndrome, is commonly seen in runners
(Figure 12.4). Pain along the posteromedial part of the leg is a common condition
I.
II.
FIGURE 12.4 Two examples of pain drawings by patients with medial tibial syndrome.
166
and accounts for 60% of all lesions causing pain in the athletes leg.22 Some authors
report normal intramuscular pressure measurements in the posterior compartments
of these patients.2325 Normal intramuscular pressures during exercise and at rest
after exercise were measured simultaneously in the flexor digitorum muscle and
the tibialis posterior muscle.26 DAmbrosia et al. found no basis for increased
intramuscular pressure in either the anterior or the posterior compartments as the
cause for shin splints.23 Davey et al. reported that the tibialis posterior muscle is
contained in an osteofascial compartment separate from the rest of the deep
posterior compartment.27 Simultaneous pressure recordings in the flexor digitorum
and tibialis posterior muscles of 28 consecutive patients with severe exerciseinduced posterior leg pain could not prove that any of these patients had the
syndrome.26 They concluded that chronic compartment syndrome was not the cause
of posteromedial leg pain. One possible reason for the controversy in the literature
is that pressure is measured by techniques that are less, or even not at all, suitable
for dynamic pressure recordings. Finally, simultaneous intramuscular pressure and
EMG recordings would exclude muscular activity as a reason for elevated intramuscular pressure.
Others believe the condition may be a chronic compartment syndrome in
the deep posterior compartment of the leg,2729 whereas still others feel it is an
overuse syndrome2326,30 which may have multiple etiologies. It has been suggested that chronic compartment syndrome is underdiagnosed.12 The syndrome
has been defined in a different way. Patients did not always have abnormally
elevated pressure on which the diagnosis of the syndrome was based. Furthermore, pressure was measured only at rest before exercise with the needle injection technique,31 a technique that is known to give erroneously high intramuscular
pressure readings.32,33
SYMPTOMS
Patients experience pain along the posteromedial border of the tibia and the posteromedial soft tissues. The pain may range from a dull, aching discomfort to an
intensive, persistent pain, which is aggravated by physical activity. The pain and
weakness are associated with running.
SIGNS
Patients have well-localized area of tenderness over the middle or distal thirds, or both,
of the posteromedial ridge of the tibia (Figure 12.4). They have no motor, sensory, or
circulatory disturbances. Many patients have excessive pronation of their feet.
CHRONIC COMPARTMENT SYNDROME

IN THE FOOT
The syndrome is most uncommon in this location. Middleton and co-workers
presented a 16-year-old girl with exercise-induced acute compartment syndrome
who had progressive pain and numbness in her feet after a day of high-impact
aerobics.34 Lokiec and co-workers presented an 18-year-old ballet dancer with
167
Compartments
of the foot
FIGURE 12.5 The foot is composed of nine compartments that may be affected by elevated
muscle pressure during exercise and at rest after exercise.
pain in both his feet induced by dancing for 10 min.35 The syndrome was described
in a 19-year-old male triathlete.36 The diagnosis is difficult because of the many
compartments of the foot (Figure 12.5).
SYMPTOMS
Patients experience pain and swelling over the longitudinal arch of the foot. They
complain of exercise-induced cramps in the plantar aspect of the foot. Walking and
ordinary daily activities cause no discomfort.
SIGNS
On examination following exercise, the midfoot is swollen over the medial aspect.
The foot is tense and tender. Symptoms subside after 10 min of rest. MRI has
revealed hypertrophy of all the muscles of the medial and central compartments of
both feet. Pressure in the two compartments was between 35 and 80 mmHg following
an exercise test that induced the clinical symptoms.

IN THE THIGH
This location of the syndrome is most uncommon. Raether et al. described a 26year-old long-distance runner who experienced intermittent claudication, weakness, and pain in the posterior compartment of the thigh after 4 miles of running.37
Next day, the thigh was aching. Elevated pressure in the posterior compartment
and the exercise-induced pain reversed after treatment by fasciotomy. In another
168
study, two patients with pain and swelling over the tensor fasciae lata muscle
had elevated intramuscular pressure and enlarged muscle compartment on computed tomography.38
Orava et al. diagnosed the chronic syndrome in nine patients over a 13-yearperiod.39 They were power lifters, body builders, and endurance walkers, and one
cyclist. Four of the nine patients had used steroids. The diagnosis was not confirmed
by intramuscular pressure recordings.
Patients complained of gradually worsening pain in the involved muscles of the
thigh. The thigh muscles were numb and weak after exercise. One patient had a
small tear of the fascia. Muscle biopsy may show superficial muscle cell necrosis.
Metabolic rhabdomyolysis, muscle strain, and poliomyelitis were a few differential
diagnoses in these cases.39 Exercise-induced medial thigh pain was diagnosed as
entrapment of the obturator nerve in 29 patients.40 Normal needle EMG demonstrated
denervation of the adductor muscles.

IN THE FOREARM
The forearm contains at least three compartments: the extensor, the superficial, and
the deep flexor compartments. Chronic compartment syndrome in the forearm seems
to be a rare condition, because only a few cases have been described following
trauma,41 routine strenuous activity,42,43 and exposure to vibrating tools.44 Diagnosis
of the syndrome demands a high level of suspicion. Competitive motor racing is a
form of excessive and continuous exercise. Rydholm et al. presented 14 patients
with effort-related pain in the dorsal compartment of the forearm. Six of them had
abnormally elevated intramuscular pressure.
SYMPTOMS
Patients experience swelling and pain in the forearm due to exercise, followed by
weakness of the flexion grip strength of the hand. They may experience pain during
passive extension of the wrist and fingers after an exercise test. Numbness and
tingling in the distribution of the median nerve after exercise have been
described.41,42 Gradual decrease in muscle strength forces patients to discontinue
exercise after a while. Symptoms fade away on stopping the activity, but recur
with resumption of activity.
SIGNS
Patients have a full range of motion in the elbow, wrist, and finger joints. Swelling,
firmness, and induration over the muscle bellies of the forearm are associated with
weakness of the hand grip after exercise.42,43,45 Muscular hypertrophy and postexercise edema of the abductor pollicis longus and extensor pollicis brevis muscles have
been described after unaccustomed strenuous exercise.46 The muscle bellies are
tender at palpation and at passive stretch immediately after an exercise test that
elicits the symptoms.
169

IN THE HAND
Chronic compartment syndrome is an unusual cause for hand pain. It has been
described in the first web space in the first dorsal interosseous muscle. The function
of this muscle is to flex the metacarpophalangeal joint and extend the proximal
interphalangeal joint of the index finger. The syndrome has been described among
hairdressers, guitar players, and stenographers.7 Chronic compartment syndrome
was diagnosed in 4 of the 15 patients with writers cramp.7
SYMPTOMS
Patients experience pain and swelling over the first web space. They experience
weakness of the pinch grip and clinical symptoms similar to patients with writers
cramp. Patients complain of exercise-induced cramping sensation in the radial side
of the dorsum of the hand.
SIGNS
At investigation following an exercise test, the first web space is swollen. Patients
may experience pain at passive stretch of the muscle. Since no sensory nerves are
found in this compartment, abnormalities related to a sensory nerve will be lacking
in this localization.7 Physical signs of hypoesthesia are not present. However, after
exercise on a work simulator,3 the peak torque for performing lateral key pinch and
three-point pinch decrease, and the time for tolerated activity decreases significantly.4
Muscle relaxation pressure during exercise7 and intramuscular pressure at rest after
exercise4,47 increase to 30 to 50 mmHg. Hand volume increased by 20 mL as assessed
by volumetry.4

IN THE LUMBAR SPINE
The lumbodorsal compartment of the lumbar spine is a relatively unyielding osteofascial space, which is the prerequisite for the chronic compartment syndrome in
the lumbar spine.4850 Chronic compartment syndrome in the muscles of the lumbodorsal compartment is extremely uncommon in patients with exercise-induced
low-back pain.8 Only 1 out of 12 patients with strictly exercise-induced paravertebral
pain in the lumbar spine had the syndrome. The syndrome occurs among patients
who have a high physical activity level, pain only during and immediately after
activity, and no neurological deficits in the legs. In a larger series of patients with
low-back pain, it was diagnosed in 7 out of 102 patients.51 Pressures during exercise
and at rest after exercise in the erector spine muscles were recorded over a 15-year
period in more than 30 patients who fulfilled all the clinical criteria for suspected
chronic compartment syndrome.8 Only five patients with chronic compartment syndrome in the lumbar spine were diagnosed. The syndrome seems to be a rare cause
of exercise-induced low-back pain.
170
Patients have paravertebral pain induced by exercise in the lumbar spine. They
have no low-back pain at rest. They are not on sick leave. At physical investigation,
they have a normal range of motion and no neurological deficits in the lower
extremities. In unilateral cases, a paravertebral swelling is visible.
ADDITIONAL DIAGNOSTIC TOOLS

Measurements of tissue oxygenation by near-infrared technique (Figure 11.4),15 by
PO2 measurements,52 or local muscle blood flow by laser Doppler flowmetry16 may
provide additional methods to diagnose the syndrome. Patients with chronic compartment syndrome have a slow or delayed reoxygenation and default hyperoxygenation following an exercise test. Measurements of local muscle blood flow by
Xenon133 should be used only when clinical research of the syndrome is performed.2
Recently, measurement of muscle blood flow by a noninvasive photopletysmographic
technique to diagnose chronic compartment syndrome was presented.53
MRI and phlebography are not useful in diagnosis of chronic compartment
syndrome. However, thallium-201 chloride scintigraphy17,18 and 99Tcm methoxyisobutylisonitrile scintigraphy have been suggested as diagnostic tools of the syndrome.54 These techniques have been reported on 46 patients who were suspected
on clinical grounds of having a chronic compartment syndrome. The sensitivity of
the test and measurements was 80%.
SUMMARY
Chronic compartment syndrome in the leg occurs in a minority of patients with
exercise-induced leg pain. A patients history of pain induced only during exercise,
occurring only in the anterior aspect of the leg, and requiring the patient to interrupt
the physical activity suggests chronic anterior compartment syndrome. Physical
examination immediately following an exercise test is most helpful. The involved
muscles are swollen, weak at testing, and tense at palpation. History and clinical
signs are helpful in selecting patients for pressure studies during or following
exercise. Near-infrared spectroscopy is a noninvasive additional tool to diagnose
the syndrome.
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4. Phillips, J.H., Mackinnin, S.E., Murray, J.F., and Mcmurtry, R.Y., Exercise-induced
chronic comparment syndrome of the first dorsal interosseous muscle of the hand: a
case report, J. Hand Surg., 11-A, 124, 1986.
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36, 1994.
7. Styf, J., Forsblad, P., and Lundborg, G., Chronic compartment syndrome in the first
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Am. J. Sp. Med., 16, 165, 1988.
11. Rorabeck, C.H., Bourne, R.B., and Fowler, P.J., The surgical treatment of exertional
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12. Detmer, D.E., Sharpe, K., Sufit, R.L., and Girdley, F.M., Chronic compartment syndrome: diagnosis, management and outcomes, Am. J. Sp. Med., 13, 162, 1985.
13. Fronek, J., Mubarak, S.J., Hargens, A.R., Lee, Y.F., Gershuni, D.H., Garfin, S.R. et
al., Management of chronic exertional anterior compartment syndrome of the lower
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14. Styf, J. and Krner, L., Chronic anterior compartment syndrome of the lower leg;
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17. Hayes, A.A., Bower, G.D., and Pitstock, K.L., Chronic (exertional) compartment
syndrome of the legs diagnosed with thallous chloride scintigraphy, J. Nucl. Med.,
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19. Garfin, S., Mubarak, S.J., and Owen, C.A., Exertional anterolateral compartment
20. Styf, J., Entrapment of the superficial peroneal nerve: diagnosis and treatment by
21. Styf, J.R. and Morberg, P., The superficial peroneal tunnel syndrome: results by
decompression, J. Bone Jt. Surg., 79-B, 801, 1997.
22. Orava, S. and Puranen, J., Athletes leg pains, Br. J. Sp. Med., 13, 92, 1979.
23. D'Ambrosia, R.D., Zelis, R.F., Chuinard, R.G., and Wilmore, J., Interstitial pressure
measurements in the anterior and posterior compartments in athletes with shin splints,
Am. J. Sp. Med., 5, 127, 1977.
24. Mubarak, S.J., Gould, R.N., Lee, Y.F., Schmidt, D.A., and Hargens, A.R., The medial
tibial stress syndrome: a cause of shin splints, Am. J. Sp. Med., 10, 201, 1982.
25. Wallensten, R., Results of fasciotomy in patients with medial tibial syndrome or
chronic anterior compartment syndrome, J. Bone Jt. Surg., 65-A, 1252, 1983.
747, 1989.
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27. Davey, J.R., Rorabeck, C.H., and Fowler, P.J., The tibialis posterior muscle compartment: an unrecognized cause of exertional compartment syndrome, Am. J. Sp. Med.,
12, 391, 1984.
28. Puranen, J. and Alavaikko, A., Intracompartmental pressure increase on exertion in
patients with chronic compartment syndrome in the leg, J. Bone Jt. Surg., 63-A, 1304,
1981.
29. Rorabeck, C.H., Exertional tibialis posterior comparment syndrome, Clin. Orthop.,
208, 61, 1986.
Med., 3, 243, 1995.
an experimental investigation using the Slit catheter, J. Trau., 21, 446, 1981.
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of bilateral feets: a case report, Ft. Ank., 16, 95, 1995.
35. Lokiec, F., Siev-Ner, I., and Pritsch, M., Chronic compartment syndrome of both
feet, J. Bone Jt. Surg., 73-B, 178, 1991.
36. Mollica, M.B., Chronic exertional compartment syndrome of the foot, J. Am. Podiat.
Med. Assoc., 88, 21, 1998.
thigh, Am. J. Sp. Med., 10, 40, 1982.
38. Rydholm, U., Brun, A., Ekelund, L., and Rydholm, A., Chronic compartmental
syndrome in the tensor fasciae latae muscle, Clin. Orthop., 177, 169, 1983.
39. Orava, S., Laakko, E., Mattila, K., Mkinen, L., Rantanen, J., and Kujala, U.M.,
Chronic compartment syndrome of the quadriceps femoris muscle in athletes, Ann.
Chir. Gynecol., 87, 53, 1998.
40. Bradshaw, C., McCrory, P., Bell, S., and Brukner, P., Obturator nerve entrapment: a
cause of groin pain in athletes, Am. J. Sp. Med., 25, 402, 1997.
of the forearm: a case report, J. Hand Surg., 10, 302, 1985.
42. Pedowitz, R.A. and Toutoungi, F.M., Chronic exertional compartment syndrome of
the forearm flexor muscles, J. Hand Surg., 13 A, 694, 1988.
43. Rydholm, U., Werner, C.O., and Ohlin, P., Intracomparmental forearm pressure during
rest and exercise, Clin. Orthop. Rel. Res., 175, 213, 1983.
44. Styf, J.R., Andersson, G., and Eriksson, K., Exposure to vibrations increases intramuscular pressure in the forearm, personal communication, 2002.
45. Wasilewski, S.A., and Asdourian, P.L., Bilateral chronic exertional compartment
syndromes of forearm in an adolescent athlete, Am. J. Sp. Med., 19, 665, 1991.
46. Solheim, L.F. and Hagen, R., Chronic compartmental syndrome of the abductor
pollicis longus andr extensor pollicis brevis muscles, Arch. Orthop. Trau. Surg., 94,
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49. Peck, D., Evidence for the existence of compartment syndromes of the epaxial
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50. Peck, D., Nicholls, P.J., Beard, C., and Allen, J.R., Are there compartment syndromes
in some patients with idiopathic back pain? Spine, 11, 468, 1986.
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13
Surgical Techniques and

Results of Treatment of
Chronic Compartment
Syndromes
INTRODUCTION
There are three options of treatment for patients with chronic compartment syndrome. The rst is to adjust the activity to a level that is pain-free. Second, patients
may try other nonsurgical treatments like nonsteroid antiinammatory drugs, diuretic
treatment, massage, and physical therapy.1 These treatments have not been successful. Third, surgical decompression by fasciotomy has been shown to give good results
in most patients.26
Bear in mind that patients may have two or more leg diseases simultaneously.
Successful treatment of one disease may not lead to full recovery, because a second
disease is left undiagnosed and untreated. Usually, patients with multiple locations
of leg pain do not have chronic compartment syndrome. Also, leg pain in patients
with disseminated chronic musculoskeletal pain is not indicative of chronic compartment syndrome.
PATHOPHYSIOLOGY OF TREATMENT
The abnormally elevated intramuscular pressure in patients with chronic compartment syndrome impairs local muscle blood ow. Patients are affected by the local
muscle ischemia. They experience premature muscle fatigue, swelling, and pain
induced by exercise. Muscle tissue normally swells during exercise. In patients with
chronic compartment syndrome, the swelling, normal or abnormal, is combined with
decreased compliance of the compartment.
The goal of treatment is to restore a painless leg with normal neuromuscular
function of the tissues in the compartment. This is achieved by fasciotomy, which
normalizes local muscle blood ow and restores perfusion pressure by decreasing
muscle relaxation pressure during exercise and intramuscular pressure at rest after
exercise. The syndrome is never associated with sequel of ischemic contracture.
Treatment by fasciotomy allows the muscle to swell without increased intramuscular pressure as a result. Fasciotomy alters the compliance of the compartment
as illustrated in Figure 13.1. Fasciotomy also increases the perfusion pressure by
normalizing the muscle relaxation pressure during exercise and intramuscular pres175
176
Pressure
Before fasciotomy
After fasciotomy
Volume
FIGURE 13.1 Compliance in patients with chronic compartment syndrome before and after
fasciotomy. After fasciotomy the muscle tissue in the compartment swell but intramuscular
pressure increases to normal levels.
sure at rest after exercise. Muscle relaxation pressure is the pressure in the relaxed
muscle between two muscle contractions.
NONOPERATIVE TREATMENT
Nonoperative treatment of leg pain includes physiotherapy, antiinammatory drugs,
and orthotics, which may play an important role in the management of patients with
exercise-induced leg pain. However, such treatment is usually not effective in the
management of chronic anterior compartment syndrome. In a pilot study, treatment
by massage signicantly increased the work performed in dorsiexion before pain
developed.1 No signicant difference in intramuscular pressure before and after
massage was found.
A trial of rest for about 1 month followed by gradual resumption of normal
activities may relieve the pain, but the symptoms often return as the athlete returns
to the same intensity level of exercise. Nonoperative treatment for up to 1 year was
found to be unsuccessful.7 Therefore, nonoperative treatment options include only
modication of the subjects activity level.
SURGICAL TREATMENT
Surgical decompression by fasciotomy or partial fasciectomy of the symptomatic
compartment is the only option available if the athlete is unable or unwilling to give
up the activity that induces the symptoms. About 50% of patients with chronic
anterior compartment syndrome in the leg have periostitis as a symptom.8 The
symptom may be induced by increased tension of the fascial insertion on the anterior
ridge of the tibia. Fasciotomy also alleviates the pull from tensile forces acting on
the anterior margin of the tibia by the fascia.
Surgical Techniques and Results of Treatment
177
LEG COMPARTMENTS
The leg is by far the most common site for the syndrome.
Surgical Technique
Several techniques have been described for decompression of leg compartments.
Different techniques use variations of skin incisions. Variations of the techniques have
been developed to decrease size of skin incisions. Some use two incisions,3,7,9 whereas
others include the use of one skin incision.46 It is important to perform complete
decompressions extending over the whole muscle compartment (Figure 13.2).
For the anterior compartment, a single skin incision of approximately 5 cm
(2 in.) in length is made over the proximal part of the middle third of the leg about
4 cm lateral to the anterior margin of the tibia.5 It may also be made more laterally
Fasciotomy
Skin incision
FIGURE 13.2 Decompression of the anterior compartment of the leg by a single 5- to 7-cmlong skin incision 3 cm lateral of the anterior margin of the tibia. By a tunnel technique, the
fascia may be divided to the Gerdies tubercle proximally and to the dorsal retinaculum distally.
178
halfway between the tibial crest and the bular shaft.10 The fascia over the anterior
tibial muscle is dissected from the subcutaneous tissue and from the subfascial tissues
all the way to the extensor retinaculum at the ankle joint and to Gerdies tubercular
at the knee joint. The fascia is incised over the tibialis anterior muscle 2 to 3 cm
lateral to the anterior margin of the tibia. Care must be taken to avoid the supercial
peroneal nerve at its distal position.5,11 The nerve pierces the fascia at the junction
of the middle and distal thirds of the leg. It often may have an anomalous course.12
Fasciotomy should include a fascial defect if present.
If two incisions are used, a suitable length is 4 cm, each 12 to 15 cm (5 to
6 in.) apart.11 Complete longitudinal release of both compartments is accomplished by a fasciotome10 or long Metzenbaum scissors. Using a meniscotome is
not recommended, as the bills of the instrument are not sufciently long to contain
the fascia during the release.5,13,14 This instrument may also damage muscle tissue.
A fascial spatula inserted beneath the fascia to be divided can protect the subfascial tissues. The spatula contains a groove that guides the cutting blades of
the cutting instrument.
Others have used two longitudinal incisions centered over the intermuscular
septum. The advantages of the two-incision technique are that it gives easier access
to the anterior and lateral compartment fascia and it is easier to conrm that the
fasciotomy is complete. Fasciotomy of the lateral compartment in addition to anterior
compartment is unnecessary to perform in patients with only chronic anterior compartment syndrome.15
Some authors recommend fasciotomy of both the anterior and lateral compartment in patients with chronic anterior compartment syndrome. Both compartments
are opened by a 4- to 5-cm-(2 in.)-long skin incision halfway between the bular
shaft and the tibial crest in the mid portion of the leg. This incision gives an easy
access to both compartments. The anterior intermuscular septum is identied and
avoided because the supercial peroneal nerve lies in the lateral compartment near
the septum.
The posterior compartments may be decompressed by a 10- to 12-cm-(4- to 5-in.)long skin incision about 3 cm posterior to the posterior margin of the tibia (Figure
13.3). By making the incision at this location, the surgeon avoids injury to the saphenous nerve and vein. Stay close to the fascia and retract the saphenous veins and nerves
anteriorly. The subcutaneous tissue is bluntly released from the fascia in distal and
proximal directions. Sometimes it may be necessary to put a ligature on the distal
venous perforant. The fascia over the exor digitorum muscle is divided all the way
to the retinaculum behind the medial malleolus. The soleus muscle is released from
the posteromedial margin of the tibia. The fasciotomy is extended proximally and then
distally till the retinaculum behind the medial malleolus is reached.
If the soleus attaches to the tibia in the distal third, it should be released from
its distal insertion on the posteromedial margin of the tibia. If the operation is done
under general anesthesia with a thigh tourniquet, the tourniquet must be released
and the homeostasis controlled before the wound is closed. Some investigators were
not able to nd a distinct fascial septum separating the tibialis posterior muscle
epimysium from adjacent deep posterior musculature,16,17 whereas others have
described the tibialis posterior muscle as a fth compartment.18,19
179
Fasciotomy
Skin incision
FIGURE 13.3 Fasciotomy of the posterior compartments. The skin incision should be placed
at least 2.5 cm (1 in.) behind the posterior margin of the tibia, and be at least 10 to 12 cm
(4 to 5 in.) long. The fascial bridge over the soleus muscle and all fascia structures attaching
to the tibia should be divided. Blind fasciotomies of the posterior compartments are not
recommended surgeons must see what they do.
Endoscopic Fasciotomy
Subcutaneous endoscopic fasciotomy may be performed through three portals 2.5 cm
(one inch) from the anterior margin of the tibia by a 4-mm diameter arthroscope (Figure
13.4). The fascia is cut with a retrograde blade for arthroscopic surgery. By repeating
the procedure at each portal, the compartment is decompressed from the level of the
bular head to the nearest point of the extensor retinaculum at the ankle joint.20
Other Techniques
Decompression of the posterior compartments has been performed through a 5-cm
incision approximately 2 cm behind the posteromedial margin of the tibia.4,6 A
double-incision technique 1 cm posterior of the posteromedial margin has also been
described.11 The need for a separate fasciotomy of the fth compartment, the tibialis
180
FIGURE 13.4 Endoscopic fasciotomy of the anterior compartment through three portals. A
retrograde blade is used to cut the fascia.
posterior compartment, has been advocated to prevent recurrences.3,4,19,21 Finally,

diathermy has been used to cut the fascia.22 Decompression of posterior compartments by blind techniques should be avoided.
Results
Pain relief for patients following fasciotomy or partial fasciectomy for chronic
compartment syndrome is well documented in the literature.2,46,11 Treatment by
fasciotomy gives good results in 60 to 100% of patients. Patients satisfaction is
generally rated 85% good or excellent results. The postoperative activity level for
patients with chronic anterior compartment syndrome is increased in 60 to 100%
of patients. Patients normalize their muscle relaxation pressure after fasciotomy.5
It therefore appears that fasciotomy, even though it does not treat the cause of the
syndrome, is still effective in eliminating the pathological increase in the compartment pressure. After fasciotomy, the contents of anterior compartment swell
but the increase of intramuscular pressure is normal. It has also been shown that
fasciotomy increases the compliance of the compartment following surgery.5,8,23,24
Fasciotomy also alleviates the pull from tensile forces acting on the anterior margin
from fascia. Most patients experience pain relief and are satised with the results
of fasciotomy. About 10% of patients may require revision surgery.5,10,25 Muscle
relaxation pressure during exercise and intramuscular pressure at rest after exercise
normalize after fasciotomy.5,8,23,24
Complications
Complication rates of 5 to 15% have been reported.2,5,11 Recurrences of the syndrome have been attributed to failure of decompression or incorrect diagnosis.
Complications include hemorrhage, wound infection, nerve entrapment and cutaneous nerve injury, and deep vein thrombosis.2,5,10,25 A lower success rate has been
reported in women after fasciotomy.26 Fasciotomy of the deep posterior compartment for leg symptoms may have a failure rate of 35%.3,6,22,27,28 Outcome of treatment by fasciotomy of the anterior compartment is better than fasciotomy of the
181
posterior compartment. One possible explanation for this is that decompression of

the posterior compartment through small incisions is not adequate. The presence
of nondecompressed compartments may cause symptoms. Another possible option
is that diagnosis of posterior leg pain is more difcult and may result in a higher
proportion of incorrect or missing diagnoses. Complications to surgery, such as
sensitivity to touch, are another explanation to suboptimal results following surgery.
FOOT COMPARTMENTS
Chronic compartment syndrome in the foot compartments is uncommon but is
becoming more recognized. Only a few cases of chronic compartment syndrome in
the feet have been reported.2932
Surgical Technique
Decompressive fasciotomy of the affected compartments is recommended. The
medial compartment is the most commonly involved.31 Bilateral decompressive
fasciotomy is performed through a 5-cm incision along the medial aspect of the
midfoot, just beneath the proximal half of the rst metatarsal (Figure 13.5). Walking
with full weight bearing is encouraged after the third postoperative day and full
activity is allowed 8 weeks after surgery if the patient is symptom-free.29,30
Results
Good results have been reported following decompression of the medial compartment of the foot.31 The majority of patients treated by decompression experience
pain relief. They are satised with the results of the operation because they can
FIGURE 13.5 Medial skin incision that is used to divide the fascial structures of the medial
and central compartments of the foot.
182
increase their level of physical activity.25 It is unclear if treatment by fasciotomy

yields satisfactory results for chronic compartment syndrome in the feet.
THIGH COMPARTMENTS
Chronic compartment syndrome is an unusual cause of thigh pain. The syndrome
has been reported in the anterior or quadriceps muscles of the thigh,33,34 the posterior
compartment,35,36 and in the tensor fasciae lata muscle.37 Modied training technique
and adjusted activity level are tried rst. Different techniques for fasciotomy of the
thigh compartments have been described.3437
Surgical Technique
The anterior compartment may be decompressed by an 8- to 12-cm-long skin incision.
The fascial incision is continued 10 cm in proximal and distal directions. The fascia
over the vastus lateralis muscle just anterior to the tractus ileotibialis may be opened
through a 8- to 10-cm (4 in.)-long skin incision. By a tunnel technique, the fasciotomy
may be extended 10 cm in a proximal and 10 cm in a distal direction.34 A surgical
drain was used for 24 h. Normal weightbearing started on the same day.
The posterior compartment is decompressed through a 6- to 12-cm-long skin
incision in the middle posterior aspect of the thigh. In tall patients, two skin incisions
may be necessary. The common femoral fascia over the biceps femoris, semitendinosus, and semimembranosus muscles is divided.36 The transversal bers of the
fascia are divided and adhesions divided bluntly with ngers (Figure 13.6). The
procedure may be performed with local anesthesia in about 50% of patients.36 The
tensor fasciae lata is opened through a longitudinal fasciotomy.37
Results
Excellent or good results following fasciotomy of the anterior compartment of the thigh
were described in all patients in a series of nine,34 and in 85% of patients with chronic
compartment syndrome of the posterior compartment.36 Biopsies from fascia were
thicker than in normal cases. Complications have been reported in 15% of patients. These
include hematoma, wound dehiscence, and local sensory dysfunction around the incision.
FOREARM COMPARTMENTS
Chronic compartment syndrome of the forearm is not very common.3842 It has been
described in the dorsal compartment43 and the volar compartments.38,41,44,45 It has also
been reported in association with the exor compartment and the anconeus muscle.46,47
The syndrome involving the anconeus muscle presents as lateral elbow pain.
Surgical Technique
Fasciotomy for chronic compartment syndrome in the forearm is carried out similarly
to that described for acute compartment syndrome. The same technique as used for
acute fasciotomy described by Gelberman et al. may be used to decompress the
183
FIGURE 13.6 Skin incision (in the left thigh) and fasciotomy (dotted lines, right thigh) of
the hamstring muscles.
extensor and exor compartments of the forearm.48 A longitudinal incision is made

over the exor muscles of the forearm (Figure 6.10 and Figure 6.11). The supercial
exor muscles are retracted laterally and the exor carpi ulnaris muscle medially.
The fascia over the deep exor muscles must also be split longitudinally.38,39,44 The
FIGURE 13.7 Fasciotomy of the rst dorsal interosseus muscle of the hand.
184
skin is sutured primarily. It is important to decompress the carpal tunnel as well. In

this way, an edge effect from the volar ligaments on the median nerve is avoided.
Chronic compartment syndrome in the exorpronator muscle group was
treated in one patient by a 3-cm skin incision. The lacertus brosus was split over
a length of 10 cm.45
Results
Decompression by fasciotomy normalizes intramuscular pressure in all patients49
and gives satisfactory results in the presented case reports.38,39,44,45,49
HAND COMPARTMENTS
Patients with exercise-induced pain over the rst interdigital cleft, resembling writers cramp, may have abnormally elevated intramuscular pressure recordings during
exercise and at rest after exercise.50 The syndrome is successfully treated by fasciotomy of the st dorsal interosseous muscle with the patient under radial nerve
block.50,51 A 3- to 4-cm-long curved skin incision is used (Figure 13.7). Compression
dressing is applied for 10 days. Full activity is allowed 2 weeks after the operation.50
Fasciotomy relieves the pain and normalizes the muscle relaxation pressure during
exercise and intramuscular pressure at rest after exercise.42,5053
LUMBAR SPINE
Chronic compartment syndrome in the paravertebral muscles is a rare reason for
low-back pain. During a 20-year period, only 12 patients with strictly exerciseinduced low-back pain were suspected, on clinical grounds, to have chronic compartment syndrome in the erector spinae muscle. Only ve of them had abnormally
elevated intramuscular pressures, conrming the diagnosis.54 Konno and co-workers
diagnosed the syndrome in 7 out of 102 patients with low-back pain.55
A 10-cm-long skin incision is made 2 to 3 cm lateral to the spinal processes and
centered at the spinous process of the rst lumbar vertebrae. The fascia covering the
paraspinal muscles is split to the sacrum and 10 cm proximal of the L1 level.54 Fasciotomy of the erector spinae muscle has relieved back pain in the few reported cases.54,55
POSTOPERATIVE MANAGEMENT
Early mobilization is recommended by most authors to prevent scarring and adhesion.5,6,11,56,57 The sutures are removed after about 2 weeks. This author prefers the
intracutaneous suturing technique. Light running is initiated and exercise is progressed as tolerated over the next 2 to 6 weeks. Others recommend ambulating by
crutches for the next 2 weeks. The rst 2 days patients are treated by adjusted
physical activity level, external compression of the leg, and stretching of leg muscles.
Patients walk by crutches for the rst 1 to 3 days. The elastic compression bandages
are released after 3 days. Full weight bearing is encouraged after 12 h and patients
are free to walk unlimited during the rst 12 days and thereafter increase their
physical activity level by jogging. Athletic activities, including competition, are
185
allowed after 6 weeks.5,13,14,5860 Return to full athletic activity usually occurs between
4 and 8 weeks.
SUMMARY
Treatment of the syndrome by fasciotomy gives good results in 60 to 100% of
patients. Patients experience a high level of pain relief, and are satised with the
outcome because they are able to increase their level of physical activity. The surgeon
must use an atraumatic technique. Surgeons must be able to see what they are doing;
there should be no blind fasciotomies in the posterior or lateral compartments. The
anterior compartment may be decompressed by limited or by multiple skin incisions.
Patients should be informed of the less favorable outcomes following fasciotomy of
the posterior compartments and complication rates of surgery. Patient selection is
important. Patients who experience leg pain as a part of disseminated chronic
musculoskeletal pain do not benet from surgical treatment.
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compartment syndrome with massage: a pilot study, Clin. J. Sp. Med., 8, 14, 1998.
2. Detmer, D.E., Sharpe, K., Sut, R.L., and Girdley, F.M., Chronic compartment syndrome: diagnosis, management and outcomes, Am. J. Sp. Med., 13, 162, 1985.
3. Rorabeck, C.H., Fowler, P.J., and Nott, L., The results of fasciotomy in the management of chronic exertional compartment syndrome, Am. J. Sp. Med., 16, 224, 1988.
4. Schepsis, A.A., Martini, D. and Corbett, M., Surgical management of exertional
compartment syndrome of the lower leg, Am. J. Sp. Med., 21, 811, 1993.
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12, 391, 1984.
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25. Howard, J.L., Mohtadi, N.G., and Wiley, J.P., Evaluation of outcome in patients
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27. Abramowitz, A.J., Schepsis, A., and McArthur, C., Medial tibial syndrome: the role
of surgery, Ortop. Rev., 23, 875, 1994.
28. Akermark, C., Ljungdashl, M., and Johansson, C., Long-term result of fasciotomy
caused by medial tibial syndrome in athletes, Scand. J. Med. Sci. Sp., 1, 59, 1991.
29. Lokiec, F., Siev-Ner, I., and Pritsch, M., Chronic compartment syndrome of both
feet, J. Bone Jt. Surg., 73-B, 178, 1991.
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31. Mollica, M.B., Chronic exertional compartment syndrome of the foot, J. Am. Podiat.
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33. Koskinen, S.K., Heinonen, O.J., and Kormano, M., Magnetic resonance imaging in
the diagnosis of chronic compartment syndrome: a case report, Clin. J. Sp. Med., 3,
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34. Orava, S., Laakko, E., Mattila, K., Mkinen, L., Rantanen, J., and Kujala, U.M.,
Chronic compartment syndrome of the quadriceps femoris muscle in athletes, Ann.
Chir. Gynecol., 87, 53, 1998.
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thigh, Am. J. Sp. Med., 10, 40, 1982.
36. Orava, S., Rantanen, J., and Kujala, U.M., Fasciotomy of the posterior femoral muscle
compartment in athletes, Int. J. Sp. Med., 19, 71, 1997.
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40. Rydholm, U., Werner, C.O., and Ohlin, P., Intracomparmental forearm pressure during
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41. Wasilewski, S.A. and Asdourian, P.L., Bilateral chronic exertional compartment syndromes of forearm in an adolescent athlete, Am. J. Sp. Med., 19, 665, 1991.
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45. Berlemann, U., Al-Momani, Z., and Hertel, R., Exercise-induced compartment syndrome in the exor-pronator muscle group: a case report and pressure measurements
in volunteers, Am. J. Sp. Med., 26, 439, 1998.
46. Abrahamsson, S.O., Sollerman, C., Sderberg, T., Lundborg, G., Rydholm, U., and
Pettersson, H., Lateral elbow pain caused by anconeus compartment syndrome: a
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50. Styf, J., Forsblad, P., and Lundborg, G., Chronic compartment syndrome in the rst
51. Phillips, J.H., Mackinnin, S.E., Murray, J.F., and Mcmurtry, R.Y., Exercise-induced
chronic compartment syndrome of the rst dorsal interosseous muscle of the hand:
a case report, J. Hand Surg., 11-A, 124, 1986.
52. Solheim, L.F. and Hagen, R., Chronic compartmental syndrome of the abductor
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14
Differential Diagnosis of
Chronic Leg Pain Induced
by Exercise
INTRODUCTION
Patients with chronic compartment syndrome may have other painful leg conditions
simultaneously. Therefore, discussion of differential diagnosis of patients with
chronic leg pain is important. Leg pain of patients has many etiologies. Each of the
leg tissues may be a source of pain. Pain may originate from bone, periost, muscle,
fascia, tendons, arteries, veins, and nerves. The tissues are closely gathered in the
leg and overlap each other. Diagnosing the causes of chronic pain in the leg may
be difcult when patients have few specic symptoms and signs at rest. Therefore,
clinical investigation following an exercise test is helpful. The test may include work
on an ergometer, running, or any specic activity that elicits the typical pain or
dysfunction in the patient.
In diagnosing the conditions, it is helpful to determine from the patients history
whether the pain is strictly exercise-induced or not. Some diseases are induced
strictly by exercise, such as the chronic compartment syndromes and entrapment of
the popliteal artery. Other diseases may give more symptoms at rest after the exercise,
such as the medial tibial syndrome and venous insufciency. Pain may occur more
randomly both at rest and during exercise, such as in nerve entrapments.
Understanding of leg anatomy, pathogenesis, and pathophysiology of leg diseases is most helpful in clinical diagnosis of the causes of chronic leg pain. History
and clinical ndings are helpful in selecting patients for pressure recording studies.
Intramuscular pressure recording and measurement of tissue oxygenation during
exercise with near-infrared spectroscopy are helpful to establish or exclude the
diagnosis of chronic leg compartment syndrome. Findings can be compared with
the symptom-free limb. Range of motion of all joints from the hip down to the foot
joints must be examined. Peripheral nerves muscles and bony prominences must be
thoroughly palpated. Pseudoradicular pain, sensory disturbances, and muscular dysfunction masquerading lumbar radiculopathy may be caused by lower-extremity
peripheral nerve entrapment.1 In a study of 150 patients with leg pain caused by
exercise, 33% had chronic compartment syndrome, 25% had stress fractures, 14%
had muscle strains, 13% had medial tibial stress syndrome, 10% had neuropathies,
and 4% had venous diseases.2 One patient had spinal stenosis. In another study on
98 patients, all of whom were suspected on clinical grounds of having a chronic leg
compartment syndrome, only 25% had the syndrome.3 In this chapter, possible
189
190
reasons for exercise-related leg pain will be discussed. The aim is to give a brief
overview of possible causes for chronic leg pain.
OVERUSE INJURIES
IN THE
LEG
Injuries resulting from overload pose major diagnostic and therapeutic problems.
The leg is, second to the knee, the most common site of pain in runners, accounting
for about 20% of all running injuries.4 Figure 14.1 illustrates the relationship between
load and tissue growth or strength. Overuse injuries by extrinsic factors such as
excessive load and training errors may induce chronic leg pain. Extrinsic factors
such as training, poor techniques, poor shoes, and inappropriate surfaces, as well as
intrinsic factors such as malalignment and muscle imbalance, may contribute to
chronic overuse injury.5 Intrinsic factors include leg length discrepancies and malalignment. The origin of plantar exor muscles on tibia may vary considerably
between individuals.6,7 Increased pronation of the feet may be associated with injuries such as the medial tibial syndrome and stress fractures. Many patients improve
or become symptom-free following thorough education about the importance of
these factors and implementation of appropriate changes.
ANTERIOR LEG PAIN

The ranges of diagnoses differ between locations. Therefore, classifying symptoms
by location, that is anterior (or anterolateral) and posterior (or posteromedial) is
helpful in diagnosing the causes of exercise-induced pain in the leg.3,8 Anterior
Tissue growth/strength
Steady state
Load
Optimal load
Hypotrophy and
degeneration
FIGURE 14.1 Relationship between load and tissue growth or strength. Steady-state load
(black dot) and optimal load level are indicated on the x-axis.
Differential Diagnosis of Chronic Leg Pain Induced by Exercise
191
Anterior
Posterior
FIGURE 14.2 Cross section of the leg. The dotted line denes anterior and posterior pain
locations in the leg. Patients history and clinical investigation are therefore valuable tools in
the diagnosis, because the range of diagnoses differs between locations.
location is dened as all the tissues located anterior to the interosseus membrane
and the posterior intermuscular septum (Figure 14.2). Painful conditions in the
anterior or anterolateral location are chronic anterior and lateral compartment syndromes, periostitis over the anterior margin of the tibia (periostalgia), peroneal tunnel
syndrome, and entrapment of the common peroneal nerve at the bular head, fascial
defects as well as stress fractures of the tibia and bula. An uncommon reason for
anterolateral pain is instability of the proximal syndesmosis.
POSTERIOR LEG PAIN

Painful conditions in the posterior or posteromedial location are the medial tibial
syndrome, chronic muscle strain injuries, accessory soleus muscle, muscular hypertension syndrome, and stress fractures of the posteromedial margin of the tibia.
Entrapment of the popliteal artery and entrapment of the tibial, sural, and saphenous
nerves are less common conditions. Pain due to venous diseases and conditions of
referred leg pain must be excluded.
SKELETAL MUSCLE PAIN

Myelinated or unmyelinated nerve bers may mediate pain in the skeletal muscle.
Muscle pain induced by exercise may be due to muscle fatigue in normal persons,
vascular insufciency, or metabolic myopathies. Other reasons include ischemic
mononeuropathy, venous dysfunction, and muscular cramps. The muscle pain may
be mechanical, inammatory, ischemic, or unknown in origin.
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Mechanical Pain
Mechanical distension of the muscle fascial envelops and other fascial structures
may be painful. One example of this is traction periostitis (periostalgia) seen in some
of the patients with chronic compartment syndrome and in patients with medial
tibial syndrome.
Inflammatory Pain
Patients with myopathies and rhabdomyolysis have constant pain and clinical ndings of tenderness, swelling, and elevated creatinine phosphokinase. Eccentric muscle activity may also induce acute muscle pain. If this is associated with chronic
pain due to partial muscle tears, the diagnosis may be very difcult.
Ischemic Pain
Ischemic pain subsides when circulation is restored, such as in chronic compartment
syndrome, intermittent claudication, and entrapment of the popliteal artery.
Miscellaneous
Calf muscle cramps induced by exercise are a common complaint in athletes.
They are triggered by contraction of a susceptible muscle. They are terminated
by passive stretching (or elongation) of the cramping muscle. The cramps are
painful and may result in muscle soreness, swelling, and impaired muscle function. The risks for muscle cramping are increased in patients with partial and
total muscle rupture.
Growing pain is a deep aching that may affect legs and thighs in children. It
may occur in up to 30% of all children.9 It may be associated with recurrent
headaches and abdominal pain. Restless legs are symptomatic in the evening and
during the early hours of the night. The symptoms are relieved by muscular activity.
Patients with venous dysfunction may experience symptoms of restless or heavy
legs. The cause of referred pain is not in the muscle.
Patients with primary bromyalgia have tender spots (or trigger points) in
muscles, ligaments, and tendon insertions. Leg pain is seldom the main complaint
in these patients.
ANTEROLATERAL LEG PAIN

ANTERIOR PERIOSTITIS (PERIOSTALGIA)
Periostitis over the anterior margin of the tibia is not a disease but a common clinical
nding of soreness possibly due to an inammatory reaction. This sign is also used
to describe those conditions that are not obvious muscle strains, myositis, tendinitis,
compartment syndromes, or stress fractures.1012 Patients with stress fractures over
the anterior margin of the tibia or chronic anterior compartment syndrome are also
painful at palpation.
193
Etiology
Pain over the anterior margin of the tibia may occur in patients with stress
fractures, myocitis, and tendinitis. Athletes are prone to get this condition when
they change the running surface and when they increase the intensity level of
their exercise. Periostitis is considered as an overuse injury. It has also been
described as a traction periostitis.
Symptoms and Signs
The pain and tenderness at palpation is located over the anterior margin of the
tibia (Figure 14.3). Periostitis occurs in about 40% of patients with anterior pain
in their legs, and from 30 to 50% of patients with chronic anterior compartment
syndrome.13 This sign alone is therefore of limited value in diagnosing the causes
of leg pain.
Treatment
Antiinammatory drugs and different methods of physiotherapy have been
described. Periostitis not responding to nonsurgical treatment may be treated by
fasciotomy of the anterior compartment in a similar way as chronic anterior com-
Stress fracture
Pain
Antero-lateral view
Medial view
FIGURE 14.3 Location of pain (light grey area) in patients with periostitis of the anterior
margin of the tibia. Patients with stress fracture (black dot) over the anterior margin have
more localized pain.
194
partment syndrome. The results of surgical treatment are inferior to those of chronic
anterior compartment syndrome.
ENTRAPMENT
OF THE
COMMON PERONEAL NERVE
The common peroneal nerve may be entrapped at the neck of the bula due to
trauma or following surgical procedures around the knee as well as the proximal
part of the lower limb.14 Entrapment of the nerve may be a more common entity
than previously recognized. It should be considered in the differential diagnosis
of exertional lateral leg pain.15 Etiology is idiopathic in most cases.16 Saal et al.
described 20 patients with entrapment of the peroneal nerve proximal to the knee
joint.1 Patients with increased sagital motion of the bular head due to rupture of
the proximal syndesmosis may experience pain and sensory dysfunction elicited
by the nerve (personal observation).
Symptoms and Signs
Leg symptoms from entrapment of the common peroneal nerve and chronic anterior
compartment syndrome can be quite similar. Patients complain of pain over the
anterolateral part of the leg and of dysesthesia, hypoesthesia, or anesthesia. They
experience foot drop or extensor weakness of the foot. The pain may radiate up into
the thigh. Reduced motor conduction velocity of the common peroneal nerve caused
by inversion damage was shown in 118 soldiers.17 At clinical investigation, patients
have a positive Tinels sign at the bular neck. The diagnosis is made on the basis
of a combination of clinical and electrophysiological ndings.
Treatment
If conservative treatment fails, the nerve may be decompressed by division of the
tendinous arch of the peroneus longus muscle.14,15 Surgical treatment should be
considered after 2 months if the patient does not recover or after 4 months if recovery
is slow.14 A thick brous arch and narrowing of the tunnel through which the nerve
passes is seen during surgery. Postoperative recovery of motor function is good in
87% of patients who had sensory and motor dysfunction before treatment. Poor
results are seen in patients who were operated on with sensory dysfunction only.16
This is also true for patients with polyneuropathy.
PERONEAL TUNNEL SYNDROME

Entrapment of the supercial peroneal nerve is a difcult diagnosis to establish
because patients often have no abnormalities on testing the neurological status at
rest. Half of the patients with peroneal nerve entrapment have a peroneal tunnel
syndrome.18 A recent report suggests that the condition is a more common cause
of anterolateral pain than reected by the literature.19 Clinical investigation following an exercise test that elicits the pain and the clinical signs is most useful.
The fourth toe exion sign can be used to identify the subcutaneous course of the
nerve at the ankle joint.20
195
Etiology
Several reasons for entrapment of the supercial peroneal nerve have been reported.
These include fascial defect and muscle herniation,21,22 lipoma,23 prolonged peroneal
tunnel,19,24 ankle sprain,25 following fasciotomy of the anterior compartment in
patients with chronic anterior compartment syndrome,3,8,13 and an anomalous course
of the nerve.19 All these etiologies can cause compression of the nerve at the site
where it emerges from the lateral compartment.
Symptoms and Signs
Patients have pain over the anterolateral part of the leg (Figure 14.4). The pain may
radiate up to the knee. Lost or disturbed sensitivity over the dorsum of the foot,
including the second to fourth toes, is a common symptom and sign of entrapment
of the nerve. Patients may also experience pain and tingling at rest when the foot
and ankle are held in specic positions, such as keeping the foot on a pedal while
driving a car. If this is the case, this position should be used when nerve conduction
studies are performed. Pain at rest is a useful symptom in diagnosing the causes,
because pain never starts at rest in patients with chronic anterior or lateral compartment syndrome.
About 50% of patients with nerve compression have a fascial defect at the spot
where the nerve emerges from the lateral compartment. This is seldom a sign of
10 to 12 cm
FIGURE 14.4 Location of pain and dysethesia in patients with entrapment of the supercial
peroneal nerve. The pain may radiate up in the thigh and down to the dorsum of the foot.
The common site for entrapment is 10 to 12 cm proximal of the lateral malleolus.
196
compartment syndrome but more often a sign of nerve compression.3 Findings from
three tests are helpful in diagnosis: (1) Pain at palpation over the anterior intermuscular septum 8 to 15 cm proximal of the lateral malleolus while the patient is
performing an active dorsiexion and eversion of the ankle joint is a sign of nerve
compression.19 (2) A positive Tinels test may also be elicited when the ankle joint
is passively exed and supinated. (3) Tinels sign rises radiating pain by local
percussion over the compression site.26 Palpation over the nerve must be performed
gently, and results of palpation must be compared to the contralateral side. As all
peripheral nerves, the supercial peroneal nerve is sensitive to pressure. Other
ndings include swelling over the anterolateral distal part of the lower leg and
decreased or even lost sensitivity over the dorsum of the foot.19,25 Fifty percent of
the patients have been reported to have normal neurographic ndings when investigated at rest.19
Treatment
Decompression by local fasciotomy22,24,25 and fasciotomy of the lateral compartment
in patients with a simultaneous chronic lateral compartment syndrome19 have been
reported to give good results in 50 to 75% of the patients. Treatment by local
fasciectomy or decompression of the peroneus tunnel without complete fasciotomy
of the lateral compartment (Figure 14.5A and B) is an alternative method of treatment
in patients who do not have a chronic lateral compartment syndrome.18
FASCIAL DEFECTS
Fascial defects occur in 20 to 60% of patients with chronic anterior compartment
syndrome8,27 and in about 5% of patients with anterior pain for other reasons.8,28
Etiology
Fascial defects may follow soft tissue trauma to the legs and after tibial and bular
fracture.8 The pain generating mechanism may be an edge effect from the rm fascial
structure on the herniating muscle tissue.
Symptoms and Signs
Patients experience pain over the fascial defect. In the standing patient, a welllocalized bulging of subcutaneous tissues is seen, which is similar to that in patients
with supercial venous insufciency.
Treatment
Symptomatic fascial defects should be treated with fasciotomy of the compartment.
The fascial incision is performed through the fascial defect. Closure of the defect
is never indicated, because it decreases the compartment size and may precipitate
an acute compartment syndrome.27,29,30
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(A)
(B)
FIGURE 14.5 (A) Intraoperative picture of partly decompressed peroneal nerve in a tunnel.
(B) Complete decompression of the supercial peroneal nerve. Arrows indicate local narrowing of the nerve.
STRESS FRACTURE
OF THE
ANTERIOR MARGIN
OF THE
TIBIA
Stress fractures in the leg comprise about 10% of all overload injuries in athletes.
Between 30% and 50% of all stress fractures in runners are in the tibia. Stress fractures
are 3 to 12 times more common in women than men. The increased risk for females
is explained by greater tension strain and strain rates in response to muscle fatigue.31
Stress fractures have been reported in about 30% of U.S. military recruits in a 14-week
period.32 The vertical ground reaction force during running may be 3 to 5 times higher,
and up to 10 times higher during jumping.33,34 These forces are absorbed 50 to 70
times/min in the running athlete. Anterior stress fractures of the tibia were rst described
in ballet dancers in 1956.35 These fractures are prone to delayed union and nonunion.
198
Stress fracture of the tibia is dened as a fracture of the bone due to its inability
to withstand nonviolent stress that is applied in a repeated subthreshold manner.
Fatigue fractures occur when abnormal stress is applied to normal bone. Insufciency
fractures occur when normal stress is applied to a weak bone.
Etiology
The causes of stress fracture may be divided into extrinsic and intrinsic factors. Extrinsic
factors are excessive body weight, poor equipment, and training errors. Training errors
may include rapid mileage increase, excessive training, and changes of surface and
equipment. Inexperienced runners sustain more injuries than experienced runners do.
Ekenman et al. found no intrinsic factor to be associated with stress fracture of the tibia.36
The etiology of stress fracture is an overload. Predictive factors are long running
distances of more than 60 to 70 km per week.37 Fifty percent of these patients run on
a hard surface. Differences in muscular anatomy may be important. Athletes with a
Type A behavior and exercise dependency have been related to tibial fractures.38 Athletes
with a Type A personality often underestimate an experienced effort and they may deny
muscle fatigue. These persons are overrepresented among athletes with stress fractures.38
Motivation, ambitiousness, and competitiveness are parts of most Type A inventories. Athletes who are scoring high on these inventories must be considered to
belong to a high-risk population for stress fractures. Leg-length discrepancy, muscular imbalance, joint laxity, presence of a cavus foot, overpronation, and Type A
personality have been suggested to be associated with overuse injuries.
Symptoms and Signs
Patients with anterior stress fracture show a slow onset of symptoms, which are exercise
related. They experience a diffuse dull pain in the leg, increasing with physical activity.
They have local pain over the anterior margin of the tibia at palpation (Figure 14.3).
On the lateral view of a radiograph, a V-shaped cut into the cortical bone and cortical
hypertrophy is visible. Bone scintigraphy is more sensitive than radiography for diagnosis of stress fracture. In some cases, lesions are asymptomatic.39
Treatment
Nonsurgical treatment includes restricted running activities. Athletes with stress
fractures over the anterior margin of the tibia heal slowly despite long immobilization periods.
In a study, surgical treatment was required in 4 out of 11 patients.40 Various
operative techniques include plating, drilling,41 and intramedullary nailing.42 Surgical
treatment by excision and bone grafting is an alternative treatment after 4 to 6 months
of failed closed treatment. Intraoperative biopsy is recommended.
STRESS FRACTURES
OF THE
FIBULA
Stress fractures of the bula occur in the distal third of the bone. Proximal bular
fractures are uncommon. The fracture is seen in runners, football players, and long
jumpers. Running on hard surfaces is more risky than running on soft surfaces.
199
Symptoms and Signs

Many patients do not experience a particular moment of onset. Symptoms come
gradually. Patients report pain to palpation over bula, local swelling, and percussion
tenderness. Most fractures are located a few centimeters proximal to the distal
syndesmosis. Radiographic ndings are positive in most patients after 4 weeks of
symptoms.43 Scintigraphy establishes the diagnosis earlier.
Treatment
Athletes heal within 6 weeks if the activity level is adjusted. Elastic support or
orthotic application may be used. Below-knee plaster is not recommended.43 Athletes
are allowed to put full weight on the leg. Activity is increased gradually as long as
pain does not recur. Stretching exercises and muscular strengthening should be
encouraged during the healing period.
TENDINOSIS
OF
EXTENSOR TENDONS
Painful areas of tendons are usually diagnosed as tendinitis, although histological

studies have not shown characteristic signs of inammatory response. The histological pattern is more characteristic of a degenerative condition. Therefore,
tendinosis may be a better and more commonly used word. In the acute phase,
an inammatory reaction may give crepitations of the anterior tibialis tendon.
Pain is elicited during passive and active movement of the ankle joint. Treatment
includes adjusted physical activity level.
INSTABILITY
OF THE
PROXIMAL SYNDESMOSIS
The condition is unusual. All patients have trauma to the leg or knee. They experience
anterolateral pain in the leg that may radiate up into the thigh (Figure 14.6). Clinical
investigation reveals that the proximal syndesmosis is unstable. Patients may have
neurogenic pain due to irritation to the common peroneal nerve, which passes around
the neck of the bula.
If physical therapy is unsuccessful, surgical stabilization of the syndesmosis is
indicated. Surgery is also indicated if patients with large sagital instability evolve
dysfunction of the common peroneal nerve with weakness of the foot extensors.
POSTERIOR LEG PAIN

Painful conditions in the posterior or posteromedial location of the leg include
medial tibial syndrome, chronic muscle strain injuries, accessory soleus muscle,
muscular hypertension syndrome, and stress fracture of the posteromedial margin
of the tibia. Entrapment of the popliteal artery and compression of the tibial,
saphenous, and sural nerves are less common conditions. Venous diseases of the
leg are very common and occur simultaneously with other painful conditions in
the leg.
200
FIGURE 14.6 Pain location of patients with instability of the proximal syndesmosis. Arrows
indicate the abnormal sagital motion of the syndesmosis. The pain may radiate proximally
and distally.
MEDIAL TIBIAL SYNDROME

The medial tibial stress syndrome is dened as an exercise-induced pain over the
middle or distal thirds, or both, of the posteromedial margin of the tibia. It is the
most common reason for posteromedial pain in the leg. It occurs simultaneously in
about 15% of patients with chronic anterior compartment syndrome and in 25% of
the patients with chronic anterior leg pain for other reasons.8,13 The condition may
cover several possible pathological conditions, which all affect the posteromedial
margin of the tibia.
Painful conditions that affect the posteromedial tissues of the leg may include
(1) tibial microstress fracture, (2) chronic periostalgia due to tension at the junction
between fascia and periost, (3) chronic compartment syndrome of the deep posterior
compartment,44,45 and (4) tendinitis and tendovaginitis.
Etiology
The syndrome is not a disease but rather a painful clinical condition without either
distinct tissue pathology or pathogenesis. It has been regarded as a periostitis in
clinical studies. There are several theories about etiology of the syndrome. Histological studies have indicated that the tissues have an inammatory reaction at the
periosteal attachment and that the bone changes are consistent with microstress
201
fractures.46 Increased bone activity with periosteal new bone formation and osteoblastic activity has been shown.46
Reneman considered that the symptoms of shin splints could constitute a mild
form of chronic compartment syndrome.47 Some have suggested that the syndrome
is caused by abnormally increased intramuscular pressure in any of the posterior
compartments of the leg,4851 whereas other studies have reported normal intramuscular pressure increase during exercise and at rest after exercise in these
patients.8,13,5254 Melberg and Styf measured intramuscular pressure simultaneously
both in the exor digitorum muscle and the tibialis posterior muscles in 28 patients
with strictly exercise-induced medial tibial syndrome.53 None of these patients had
abnormally elevated intramuscular pressure during exercise or at rest after exercise,
indicating a compartment syndrome.
Other etiologies include a short tibialis posterior tendon.55 Tight muscle tendons
are more susceptible to strain.56 Saxena et al. showed that the tibialis posterior muscle
extended much more distally than previously described.55 It is therefore likely that
contracture of the tibialis posterior muscle may cause and maintain a secondary
contracture of the exor digitorum longus muscle by virtue of their crossing. On
the other hand, anatomical dissections demonstrate that the sites of tenderness to
direct palpation over the posteromedial border of the tibia and increased activity on
bone scan correlate better with the soleus bridge overlying the deep posterior compartment than the posterior tibialis muscle.57
The soleus muscle is probably the major contributor to possible traction, which
may induce medial tibial syndrome.58 It has been found that both the soleus and the
exor digitorum longus muscles arise on the medial border of the tibia at the site
of symptoms of the media tibial syndrome. Excessive foot pronation is seen in many
patients with medial tibial syndrome.57,59 This has been correlated with forefoot
pronation and overuse syndromes in the lower extremity.60
Symptoms
Symptoms and signs of medial tibial syndrome are so typical that the diagnosis can
most of the time be made by clinical investigation. Patients complain of pain along
the middle or distal thirds, or both, of the posteromedial ridge of the tibia (Figure
14.7). The pain may occur soon after the start of exercise. On average, patients with
medial tibial syndrome experience leg pain after 200 m of running, compared to
3.5 km (ca. 2 mi) in patients with chronic anterior compartment syndrome. Leg pain
in patients with medial tibial syndrome may even be relieved by continued running,
whereas it forces the athlete with chronic anterior compartment syndrome to stop
running. In some patients, pain starts at rest after exercise and some may have more
pain the following day. The pain is less focal than in a patient with a stress fracture.
It may vary from dull ache to intense pain.
Clinical Examination
At investigation, the tenderness is located in the middle third or the middle and distal
thirds of the posteromedial margin. Often the most painful area is centered on the
202
Stress fracture
FIGURE 14.7 Pain location of patients with medial tibial syndrome. The dot indicates the
location of the stress fracture. The light gray area shows localized pain and swelling of patients
with a stress fracture of the postromedial margin of the tibia.
junction of the middle and distal thirds. The pain is aggravated on active plantarexion and supination of the ankle joint against resistance. No sensory, motor, or
vascular abnormalities have been reported. Many of these patients have excessively
pronated feet.
Plain x-ray lms are normal or may show diaphyseal cortical hypertrophy.
Scintigraphy may show a diffuse and varied intensity uptake along the length of the
posteromedial margin of the tibia.57 The uptake on the positive bone scan is quite
diffuse and different from that of a stress fracture.61,62 There is a moderate increase
of radionuclide along about one third of the posteromedial border of the tibia on
delayed images. In stress fractures, the length of the increased radionuclide activity
along the tibia is much shorter. The scintigraphic pattern can be used to differentiate
medial tibial syndrome from stress fractures.62 Allen and co-workers showed that
75% of patients with medial tibial syndrome and 20% of patients with chronic
anterior compartment syndrome had a positive 99Tcm-MDP bone scan.61 They concluded that bone scans were a useful diagnostic tool in the differential diagnosis of
exercise-induced leg pain.
Treatment
Nonsurgical treatment includes adjusted activity level and alternative activities such
as bicycling, swimming, as well as even rest combined with NSAID initially. In
severe cases, rest from running is mandatory. Physiotherapy, orthotic applications,
and NSAID must be properly prescribed before surgery is considered. Patients who
have short muscles are referred to physiotherapy. Short muscles are more susceptible
203
to strain.56 This is especially important in patients with pronated feet. Up to 30% of

patients may improve by static or dynamic orthotics. If the runners limb alignment
indicates a varus heel, treatment by a medial heel wedge may be indicated.5 A great
deal of art is involved in the management of an athlete with medial tibial syndrome.
It is important to teach patients to listen to their legs and adopt realistic goals and
timetables. Proper advice regarding running technique, shoes, and surfaces is a
challenging pedagogic duty.
Surgical treatment is not the mainstream treatment. Nonsurgical treatment is
recommended for at least 6 months because the prognosis by conservative treatment
is good. At surgery, the author follows the principles outlined by Michael and
Holder.57 The operation is performed in a bloodless eld with a thigh tourniquet.
The risk for damaging nerves and veins is much more pronounced than in surgery
on the anterior compartment. Therefore, the author recommends the use of an at
least 10-cm-(4 in.)-long skin incision, about 3 cm (1 to 1.5 in.) behind the posteromedial margin of the tibia. The veins and the saphenous nerve branches are elevated
anteriorly. In many patients, the attachment of the soleus muscle to the tibia (or
soleus bridge) must be detached to allow for fasciotomy of the deep posterior
compartment. The tourniquet is released and the homeostasis is controlled carefully
before the wound is closed by intracutaneous sutures. Surgery relieves the tension
of the fascial insertion on the tibial bone and increases compartment volume. Results
of surgery are reported as good or excellent, between 30 and 80%.44,63,64
MUSCLE STRAIN INJURY (TENNIS LEG)

Strain injuries to muscle are common. They may occur during ordinary running, but
more often during a powerful eccentric muscular contraction.56 The condition is
known as tennis leg and may cause a bothering disability.
Etiology
The painful condition is caused by a strain injury to muscle. It may include rupture
of bers of the medial head of the gastrocnemius muscle. These muscle bers are
fast twitch as opposed to the soleus muscle bers, which are primarily slow twitch.
Muscle strain injury often occurs at the myotendinous junction unless the muscle
has suffered previous compression injury leading to failure within the muscle.65
The gastrocnemius muscle is more vulnerable because it passes by both the knee
and ankle joint. The mechanism of injury includes overstretching of this muscle by
a combination of forced ankle dorsiexion and knee extension. The same injury
mechanism may also create an Achilles tendon rupture. In some patients who have
been exposed to repeat muscle strains, the clinical picture may become more complex.
Symptoms and Signs
Patients may report sudden acute calf pain during running. Some of them experience a sudden sound as if someone had kicked them in the calf. Pain and calf
swelling develops during the following 24 to 48 h. This history is important to
document initially. Repeated sudden onset of acute pain during running is a key
204
nding in the history that speaks against chronic compartment syndrome in the
leg. During this time period, patients may have had repeated strain injuries to the
calf muscles. Patients with chronic pain following partial calf muscle ruptures
complain of local deep muscular tenderness. They may experience muscle cramps
during and after exercise.
At investigation, patients may have a positive Hohmans sign, which is calf pain
during passive dorsiexion of the ankle joint. The pain may also occur during active
dorsiexion. Flexor tendons may be short. Point tenderness is found over the musculotendinous portion of the gastrocnemius muscle bellies. Ultrasonography or MRI
can be used to evaluate the extent of muscle injury. Athletes with leg weakness can
be tested with a kinetic computerized ergometer.
Treatment
In the acute phase, patients should be treated by a supportive wrap and ice application. Crutches are helpful during the rst 3 days, if necessary. A heel lift for 2 to
4 weeks before patients return to full activity is recommended. Weight bearing is
slowly increased. Calf muscle stretching and strengthening exercises are important.
When muscle strength is 90% of the noninjured side, patients may resume sports
activities. Nonsurgical treatment, including stretching and relief of the posterior
structures by foot orthotics, is helpful in most patients. Surgery for chronic cases is
not in the mainstream of treatment and should be avoided.
ACCESSORY SOLEUS MUSCLE

Symptomatic accessory soleus muscle is one of the supranumerous muscle belly
syndromes. Patients have an extra soleus muscle belly and a tendon that inserts
on the calcaneus or to the Achilles tendon.6668 The incidence of an accessory
soleus muscle ranges between 0.7 and 5.5%.69 The accessory soleus muscle can
vary in its anatomic conguration. The exor digitorum longus muscle may also
have an accessory muscle belly.70 In these patients, the tibial nerves were compressed by the muscle.
Pathophysiology may be diminished blood ow leading to ischemic pain.67,69
Exercise-induced compartment syndrome and compressive neuropathy of the tibial
nerve have been suggested.71 Others have suggested that the pain comes from fascial
traction on the periosteum.68
Symptoms and Signs
Patients experience burning pain and persistent swelling, which is accentuated during
and after exercise over the distal third of the posteromedial part of the leg, including
the tarsal tunnel. The pain may radiate distally into the longitudinal arch of the foot.
Asymptomatic swelling occurs in about 25% of patients. Intramuscular pressures
during exercise and at rest after exercise are increased in these patients, but not to
the level seen in chronic compartment syndrome. The condition may be evaluated
by ultrasound, CT, or MRI. On MRI imaging, the accessory soleus muscle may
insert into the calcaneus in ve different ways.72,73
205
Pressure
A.
B.
C.
FIGURE 14.8 (A) Patients with muscular hypertension syndrome have normal muscle contraction pressure and muscle relaxation pressure during exercise. (B) At rest after exercise,
patients are unable to relax their leg muscles. Therefore, the pressure is abnormally elevated
and can be interpreted as chronic compartment syndrome. (C) Short, sometimes repeated,
periods of low pressure indicate that the patients are unable to relax their muscles. This
condition is not based on a real volume load of the muscle.
Treatment
Fasciotomy has been reported to be successful.69 Treatment may also include excision of the supranumerous muscle or muscle belly.66,67 Excision should be reserved
for those patients who do not respond to fasciotomy.69
MUSCULAR HYPERTENSION SYNDROME

This syndrome may easily be judged as a chronic compartment syndrome because
intramuscular pressure is abnormally elevated at rest after exercise. However, intramuscular pressures during muscle contraction and muscle relaxation during exercise
are normal (Figure 14.8). The patient is unable to relax the leg muscles completely
initially at rest after exercise.13 The condition has also been described as tension
myalgia.74 For example, patients with low-back pain were found to have EMG
activity at rest.75 A rare condition of muscle stiffness and spasm was described in
14 patients over a time period of 32 years.76
Symptoms and Signs
Patients with muscular hypertension syndrome have pain during exercise and at rest
after exercise. They are not able to relax their calf muscles at rest after exercise.
Intramuscular pressure at rest after exercise is elevated because of an active remaining muscle contraction.13 The EMG signal is positive. When the signal turns silent,
the intramuscular pressure also normalizes. Some patients may have muscle pain in
other locations, although leg pain is dominating.
206
Treatment
Treatment by fasciotomy is not helpful. However, stretching and muscle relaxation by biofeedback have been encouraging. Treatment by stockings, which
give external compression of 15 to 22 mmHg, is helpful in patients with simultaneous venous insufciency.
STRESS FRACTURES
OF THE
POSTEROMEDIAL MARGIN
OF THE
TIBIA
In athletes, the tibia is the most common site for stress fracture. Tibial fractures are
involved in up to 50% of all stress fractures. The overall incidence of stress fractures
in an athletic population is 0.12%.77 In a population of runners, the incidence has
been reported to range from 4 to 16%.41,77 The risk for a tibial stress fracture in
women is greater. Stress fractures may be multiple. They include all areas of the
tibia. When located in the proximal or distal third of the tibia, they are found on the
posteromedial ridge of the bone. These fractures develop slowly, which allows for
adequate bone remodeling and hypertrophy.
Etiology
The development of a stress fracture is multifactorial. It is related to the level and
intensity, duration, and type of physiological activity, sex, bone size and mineralization, and the athletes personality. Risk factors include running on hard surfaces,
inadequate shoes with poor impact-absorbing quality, and, nally, lower-limb malalignment. Intrinsic factors are forefoot varus, subthalar varus, tibia vara, leg-length
inequalities, and pes cavus.41,77
Pathogenesis
According to one theory, muscle fatigue and weakness may reduce the relative shockabsorbing capabilities of muscles in the lower extremities. The reason for this is the
higher tensile forces in the bone when muscle fatigue occurs.31 According to another
theory, the tight forces across bones generated by rhythmic muscular activity may
cause mechanical insult, resulting in fatigue fracture. If repetitive overload continues,
the weakened cortex may fracture completely. In early stages of stress fractures, an
increased number of erythrocytes are found within bone, resulting in vascular congestion and thrombosis. Subsequently, osteoclastic reposition and periosteal new
bone formation by osteoblasts take place.
Symptoms and Signs
Stress fractures of the tibia cause local tenderness and subcutaneous swelling (Figure
14.7). Radiographic examination is positive in 90% of the patients within 1 month.
Radiographic examination and bone scans are normal in patients with chronic anterior compartment syndrome.54
207
Treatment
Most tibial stress fractures heal without surgical treatment. Nonsurgical treatment
includes restricted running activities.
ENTRAPMENT
OF
POPLITEAL ARTERY
Entrapment of the popliteal artery caused by anatomic variation of blood vessels and
muscles in the popliteal fossa was described by Stuart in 1879. The prevalence of the
syndrome has been reported to be 0.17 to 3.5% in cadaver studies. The incidence of
popliteal artery entrapment is up to 3.5% in cadaver dissection.78 Darling et al. believed
that the syndrome was commonly overlooked although it is unusual.79 Absence of the
posterior tibial artery has been reported in 0.5 to 2.5% of extremities.80
Etiology
Patients with entrapment of the popliteal artery have an abnormal anatomical relationship between the artery and surrounding soft tissues. The artery may be entrapped
under the medial gastrocnemius head or have an anomalous course (Figure 14.9). The
popliteal vein may follow the anomalous course of the artery.78 Intimal hyperplasia
may occur as a result of endothelial injury. Intramuscular pressure during exercise is
not elevated in patients with entrapment of the popliteal artery.81 The disease is possibly
more common than reected in the literature. However, the patients symptoms resemble those of chronic compartment syndrome and may be misdiagnosed.70,82,83
Tibial nerve
Popliteal artery
Gastrocnemius muscle
Medial
Lateral
FIGURE 14.9 Entrapment of the popliteal artery. The artery has an anomalous course medial
to the medial head of the gastrocnemius muscle. The artery may also run through the medial
head of the muscle.
208
Classification
There are many variations of how the medial head of the gastrocnemius muscle
entraps the popliteal artery.84 Represa et al. classied entrapment of the popliteal
artery into three types:85 (1) Type 1. The popliteal artery passes medial to the medial
head of the gastrocnemius muscle. This is the most common type (63%). (2) Type
2. The popliteal artery cuts across the medial head of gastrocnemius (23%). Type 3.
The artery passes deep to the popliteal muscle (7%). In the remaining cases, the
abnormality was not categorized. Structures compressing the popliteal artery in 296
limbs were described by Stipa et al.84 Both legs were involved in 20% of cases.86
Symptoms and Signs
Patients are symptom-free at rest but the knee may feel warmer. The foot may be
cold. Young athletes may have calf cramping after exercise. Many nonathletes may
not experience symptoms, possibly because of the low activity level. Others experience progressive calf pain on walking. The typical history is intermittent claudication in the leg and foot. Pain is typically located to the level of the musculotendinous junction in the calf and may extend into the foot.
Results of physical examination with the patient at rest are usually normal. Maximal active dorsiexion or plantarexion of the ankle joint decreases muscle blood
ow in the leg and diminishes or obliterates pulses in the leg. Measurement of local
blood ow by Xenon133 shows decreased local blood ow. Measurement of muscular
oxygenation by near-infrared spectroscopy shows decreased oxygen tension.
Examination with Doppler sonography reveals decreased pulses in the tibialis
posterior and dorsal foot arteries in their resting state but more often with passive,
or active, dorsiexion of the ankle joint with the knee hyperextended. Active plantarexion of the ankle joint and ipsilateral knee hyperextension is another provocative test of the popliteal artery function. Evaluation includes Doppler ultrasonography, either with the continuous wave technique or a color Doppler, treadmill
exercise testing, and pulse volume recording. Intramuscular oxygenation decreases.
Intramuscular pressures during exercise and at rest after exercise are normal.81,82
Angiography should be done only prior to surgery. It should not be the rst choice.
MRI may be an alternative possibility.
Except chronic compartment syndrome, differential diagnosis should include
Burgers disease and arteriosclerosis. Other etiologies may be external compression
from stockings or knee braces. Also, adductor canal compression may induce leg
and foot ischemia. These patients have a history of burning pain and loss or diminished pulses of the dorsalis pedis and posterior tibial artery. 87 Young athletic patients
with exercise-induced leg pain, cramping, and neuritic symptoms may thus have a
more proximal lesion.
Treatment
The syndrome must be treated by surgery. Results are better if patients were treated
early by division of musculotendinous tissues (90% good results). When arterial
grafting is required, the long-term patency rate is about 60%.88 A posterior Z-incision
209
is made, which allows for a complete exposure of the artery and its surrounding
structures. Treatment in the early stages can often be performed by release of the
gastrocnemius anomaly. It has been demonstrated during surgery that by plantarexing
the foot, the distal pulses disappear and a brous band visibly occludes the popliteal
artery. Removal of the band restores normal blood ow to the limb. Other intraoperative
ndings include the vessels through a common ligamentous and muscular tunnel,
which is formed by a wide head of the gastrocnemius muscle.79 In late cases, the artery
may undergo thrombosis or wall deterioration. In these cases, excision of the damaged
section and grafting with a saphenous vein graft are indicated.
ENTRAPMENT
OF THE
TIBIALIS NERVE
Entrapment of the tibial nerve in the tarsal tunnel is well recognized whereas other
compression sites of the nerve are rare. Patients with pseudoradicular pain and
sensory disturbances in the foot may have lower extremity peripheral nerve entrapment.1 The popliteal artery, veins, and the tibial nerve pass through the tendinous
arch, which is formed by the soleus and popliteus muscles. Symptoms from nerve
compression at this site are very uncommon. The numbness, tingling, pain, and
paresthesia seen in patients with entrapment of the popliteal artery have been ascribed
to ischemia from arterial compression. However, Saal et al. described nine patients
with tibial nerve entrapment in the popliteal space.1
Etiology
The nerve may be entrapped at the tendinous arch of the soleus muscle89 or occur
simultaneously in patients with entrapment of the popliteal artery (Figure 14.9).84 It may
also be compressed by the medial head of the gastrocnemius muscle.84,90,91 The most
common site of entrapment at surgery is the hypertrophied medial gastrocnemius muscle.
Fibrosis of the posterior knee joint capsule has also been described.1 The tibial nerve
may also be compressed by an accessory exor digitorum muscle at the tarsal tunnel.70
Symptoms and Signs
Patients may experience burning pain that radiates up in the thigh and down into
the longitudinal arch of the foot. They have severe calf pain similar to sciatica. They
experience decreased sensitivity over the sole of the foot, weakness of the exor
hallucis longus and exor digitorum muscles, while the Achilles tendon and plantarexion force is normal. Calf pain is aggravated by active plantarexion of the
ankle joint or passive ankle joint extension. This suggests that the lesion is located
in the leg rather than the foot.
At the entrapment site, Tinels sign and tenderness at palpation are positive in
90% of the patients, whereas other neurologic signs and decits such as a positive
straight leg raising test are found in about 40% of the patients.1,90 EMG of the exor
muscles show denervation potentials.
Additional diagnostic methods including CT, MRI, and electromagnetic studies
are helpful in diagnosing this condition.89 Nerve conduction velocity is decreased
in about 80% of the patients.1
210
Treatment
The nerve is decompressed through a complete exposure.1,84,92
ENTRAPMENT
OF THE
SAPHENOUS NERVE
The saphenous nerve is a sensory branch of the femoral nerve. It passes through
the adductor canal in the thigh. The canal is surrounded by the sartorius, vastus
medialis, and adductor Magnus muscles. In the leg, the nerve is accompanied
by the saphenous vein. Entrapment of saphenous nerve may simulate vascular
disease93 and radiculopathy.1,94 Furthermore, lower extremity nerve entrapment
may mimic lumbar pain syndromes in 50% of the cases. Seventy percent of
patients with entrapment of the saphenous nerve at the adductor canal of the
thigh have leg pain.1 The condition may mimic other diseases, which affect the
posteromedial part of the leg.
Etiology
Trauma to the adductor canal and vascular surgery are the most common causes for
saphenous nerve dysfunction.95,96 Entrapment under the sartorius muscles in a bodybuilder and compression by a meniscal cyst have been reported.95 Traction on the
nerve at the site where it exits the adductor canal may cause local inammation and
edema. The nerve may also be compressed by a pes Anserinus bursitis.97
Symptoms and Signs
Most patients experience anteromedial knee pain, which may radiate into the
medial aspect of the leg following the saphenous nerve distribution (Figure
14.10).95 They may experience medial leg pain, which is similar to the pain patients
with medial tibial syndrome experience. The patient experiences burning pain,
which may be aggravated by exercise. The pain may awaken the patient at night.
It may simulate intermittent claudication, sensation of fatigue, and heaviness of
the leg.93 The pain may even mimic tears of the medial meniscus and a stress
fracture of the tibia.97
At clinical examination, Tinels sign and tenderness at the lesion site are positive
in all patients, whereas other neurologic decits distal to the compression site are
found in about 50% of the patients.1,95 The patient experiences point tenderness at
palpation over the site of entrapment or compression. This may include pressure
over the adductor canal, which induces radiating pain down to the medial malleolus
of the ankle joint. Peripheral nerve block at the adductor canal is useful in differentiating peripheral nerve pain from a spinal source.1 Electrophysiologic data indicate a side-to-side decrement of SNAP amplitude in 60% of patients.93
Treatment
Adjusted physical activity level is often sufcient. It has been suggested that
abnormal retrograde nerve impulses may be inhibited by local anesthesia.98 Saphenous nerve block at the adductor canal by a 10 mL (cc) solution of bupivacaine
211
Adductor canal
FIGURE 14.10 Location of pain and sensory dysfunction of patients with entrapment of the
saphenous nerve.
(0.25%) and 25 mg of triamcinolone diacetate in a 9:1 ratio had a favorable

outcome in 80% of patients. Seven percent of patients had increased pain after
this treatment.95 In another study, only 38% of patients reported favorably by
corticosteroid treatment.93 The length of symptoms before treatment increased the
risks for increased pain intensity at follow up. Treatment by partial release of the
sartorius muscle has been suggested. Saal and co-workers recommended treatment
by neurolysis at the site of compression between the vastus medialis and adductor
Magnus muscles.1
ENTRAPMENT
OF THE
COMMON SURALIS NERVES
The anatomical course of the sural nerve may vary. The lateral sural nerve pierces
the fascia in the popliteal fossa dorsal to the bular head. It may be entrapped
anywhere along their course. The common sural nerve runs between the heads of
the gastrocnemius muscles and pierces the fascia in the middle third of the leg. It
runs close to the Achilles tendon and within a couple of centimeters posterior and
inferior to the lateral malleolus.
Etiology
It may follow recurrent ankle sprains and calcaneus fractures,99 ganglion from the
peroneal tendons in the distal part of the leg, as well as other types of trauma to the
nerve along its course. Dorsal extension and inversion of the ankle joint may lead
to a traction injury to the nerve. Other etiologies include Bakers cysts,100 external
compression,101 and trauma.102
212
Symptoms and Signs

Patients have a subacute onset of a neuritic type of pain, including burning, tingling,
or radiation. They experience diminished sensation with or without paresthesia along
the distribution of the sural nerve in the leg and the foot.103 Pain may radiate
proximally into the calf.
Local tenderness and a positive Tinels sign along the entrapment site of the
nerve are found at clinical investigation. Patients with entrapment of the sural nerve
may have pain, tenderness, and swelling behind the lateral malleolus. Pressure over
the entrapped nerve may cause discomfort along the lateral border of the foot.103
Treatment
Decompression by removal of Bakers cysts may help recovery. Local fasciectomy
or fasciotomy at the site where the nerve emerges the fascia may help. Alternative
exercises, injections of local anesthetics, massage, nonsteroid antiinammatory
drugs, and shoe modications have been tried.
VENOUS DISEASES OF THE LEG

Return of venous blood from the lower extremity to the heart is maintained by a
series of interconnected venous muscle pumps from the foot to the thigh.104,105 During
weight bearing and muscular action, blood is expelled from the calf veins into the
thigh veins. This action depends on competent valves in the veins. More than 90%
of swollen legs seen in general practice are due to incompetence of the venous
system.106 Most people have only mild or no symptoms. Deep venous insufciency
may follow deep venous thrombosis in 70% of the patients.
VENOUS INSUFFICIENCY
Many patients with calf pain have venous insufciency. Advanced cases of deep
venous insufciency are often referred to as a postthrombotic syndrome. The main
pathophysiological factor in these patients is valvular dysfunction or venous dilatation in the deep veins. Intravenous pressure in the foot may be up to 100 mmHg. It
decreases to below 30 mmHg following activation of leg muscles. Competent venous
valves are a prerequisite for the decrease of intravenous and intramuscular pressures.105,107 The total leg volume is increased in limbs with venous insufciency. The
lling speed increases signicantly. Doppler sonography and plethysmography are
helpful investigations to reach diagnosis.
Symptoms and Signs
Patients complain of pain and ache. The legs may feel heavy and they may be restless
at night. At physical examination the legs may be swollen and show marked skin
changes such as hyperpigmentation. Elderly patients may develop ulcers. At physical
examination, patients experience a calf tenderness and a positive Hohmans sign.
Patients experience diffuse aching in the legs, which may be worse after standing.
213
The legs hurt at night. Patients may experience calf pain and muscular cramps. They
have more pain at rest after exercise than they experience during exercise. Intramuscular pressures during exercise and at rest after exercise are elevated, but not to the
level seen in patients with chronic compartment syndrome.
Treatment
Compressive stockings are the method of choice initially. Surgery for patients who
suffer from both medial tibial syndrome and venous insufciency should not be the
mainstream, because venous rheology may become considerably impaired following
fasciotomy, and the risks for an inferior surgical outcome are increased. Low-grade
compression stockings, which generate up to 15 to 22 mmHg of pressure are
sufcient for most patients. This treatment enhances the calf muscle pump leading
to decreased venous pressure. Local excision of varicose veins combined with
postoperative compression stockings for extensive time periods is helpful.
VARICOSE VEINS
Patients have diffuse leg aching, which may worsen after standing. They complain
that their legs hurt or are restless when they go to bed at night. Pain is not localized
to any specic muscular compartment. Patients repeatedly treated by local extirpations and vein stripping may develop elevated intramuscular pressure during exercise
and at rest after exercise. Only rarely are chronic compartment syndromes seen in
these patients. The condition is treated with use of compressive stockings.
VENOUS CLAUDICATION
Patients experience calf pain while walking. The condition is sometimes difcult to
differentiate from intermittent claudication due to arterial insufciency. Venous
claudication may follow thrombosis or incompetent valves of the deep veins.
THROMBOPHLEBITIS
Thrombophlebitis is a common cause of leg pain due to low-intensity exercise. The
leg may be edematous. The diagnosis is documented by venography. Patients experience leg tension at speedy walk, due to high intravenous pressure. Treatment
includes anticoagulants for 3 months. The patient should be referred to a specialist
for additional investigation of risk factors.
EFFORT-INDUCED VENOUS THROMBOSIS

The condition is uncommon. It has been associated with extensive muscular activity
in runners,108 kick boxers,109 and in football players.110 It has been seen in patients
with underlying anatomical abnormality.111 The patient experiences sudden onset of
leg pain and swelling, similar to the symptoms of patients with partial rupture of
the gastrocnemius muscle. Clinical ndings include a positive Hohmans sign and
point tenderness over the calf. The diagnosis is conrmed by ultrasonography or by
phlebography. The condition is treated by anticoagulation therapy.
214
MISCELLANEOUS
Several conditions such as inammatory reactions, lumbar disc herniation, pain after
fractures of the tibia, intramuscular lipoma in the lateral compartment, and supranumerous muscle belly syndromes may mimic the symptoms of chronic anterior
compartment syndrome in the leg. Exercise including eccentric muscle contractions,
e.g., downhill running, causes the greatest degree of delayed muscle soreness with
pain, swelling, and tenderness (Armstrong, 1984; Fridn, 1984). Runners in this
situation may even have increased intramuscular pressure at rest up to 24 h following
exercise. Eccentric exercise increases water content by 3% more than concentric
exercise and results in a higher intramuscular pressure at rest after exercise (Fridn
et al., 1988). The contractile apparatus can be damaged by eccentric exercise (Armstrong, 1984; Fridn, 1984). Repeated episodes of muscle soreness, as a reason for
chronic pain in the leg, have not been established. Increased local muscle spasms,
as veried by quantitative EMG recordings, may be one reason for chronic muscle
pain (DeVries, 1966).
COMBINED SYMPTOMS
Each tissue of the leg, including bone, periost, muscle, fascia, tendon, ligament,
arteries, veins, and nerves, may be a source of pain. All the tissues may participate in the generation of symptoms of the painful leg simultaneously in patients
with overuse injury. In some patients, several tissues may simultaneously contribute to pain generation. The medial tibial stress syndrome may sometimes
occur with deep venous insufciency or with chronic anterior compartment
syndrome. Chronic anterior compartment syndrome may occur with the peroneus
tunnel syndrome. Achilles tendinitis is a common overuse injury causing posterior leg pain. It may occur simultaneously with other conditions giving posteromedial leg pain.
SUMMARY
Leg pain in athletes has many etiologies. Each of the leg tissues may be a source
of pain. The ranges of diagnoses differ between location. Therefore, classifying
symptoms according to pain location, anterior and posterior, is helpful. A careful
history including pain analysis is important. Pain induced strictly by exercise is
indicative of chronic compartment syndrome. Pain with multiple locations in
the leg that starts soon after exercise and allows the athlete to continue running
despite pain does not indicate the syndrome. Painful conditions that cause
anterior leg pain include chronic anterior compartment syndrome, anterior periostitis, entrapment of the peroneal nerves, fascial defects, stress fractures of the
anterior margin of the tibia, extensor tendinosis, and instability of the proximal
syndesmosis. Painful conditions that cause posterior leg pain include medial
tibial syndrome, tennis leg, accessory soleus muscle, muscular hypertension
syndrome, entrapment of the popliteal artery, tibialis, saphenous and suralis
nerves, as well as venous diseases.
215
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67. Romanus, B., Lindahl, S., and Stener, B., Accessory soleus muscle: a clinical and
radiographic presentation of eleven cases, J. Bone Jt. Surg., 68-A, 731, 1986.
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68. Sekiya, S., Kumaki, K., Yamada, T.K., and Horiguchi, M., Nerve supply to the
accessory soleus muscle, Acta Anat., 149, 121, 1994.
69. Brodie, J.T., Dormans, J.P., Gregg, J.R., and Davidson, R.S., Accessory soleus muscle:
a report of 4 cases and review of literature, Clin. Orthop., 337, 180, 1997.
70. Sammarco, G.J. and Conti, S.F., Tarsal tunnel syndrome caused by an anomalous
muscle, J. Bone Jt. Surg., 76-A, 1308, 1994.
71. Trosko, J.J., Accessory soleus: a clinical perspective and report of three cases, J. Ft.
Surg., 25, 296, 1986.
72. Ekstrom, J.E., Shuman, W.P., and Mack, L.A., MR imaging of accessory soleus
muscle, J. Comp. Assis. Tomog., 14, 239, 1990.
73. Yu, J.S. and Resnick, D., MR imaging of the accessory soleus muscle appearance in
six patients and review of the literature, Skel. Radiol., 23, 525, 1994.
74. Stonnington, H.H., Tension myalgia, Mayo Clin. Proc., 52, 750, 1977.
75. deVries, H.A., EMG fatique curves in postural muscles: a possible etiology for
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76. Moersch, F.P. and Woltman, H.W., Progressive uctuating muscular rigidity and
spasm ("stiff-man" syndrome): report of a case and some observations in 13 other
cases, Staff Meet. Mayo Clin., 31, 421, 1956.
77. Orava, S. and Puranen, J., Athletes leg pains, Br. J. Sp. Med., 13, 92, 1979.
78. Gibson, M.H.L., Mills, M.S., Johnson, G.E., and Downs, A.R., Popliteal entrapment
syndrome, Ann. Surg., 185, 341, 1977.
79. Darling, R.C., Buckley, C.J., Abbott, W.M., and Raines, J.K., Intermittent claudication
in young athletes: popliteal artery entrapment syndrome, J. Trau., 14, 543, 1974.
80. Zwass, A. and Abdelwahab, I.F., A case report of anomalous branching of the popliteal
artery, Angiology, V, 132, 1986.
81. Bell, S., Intracompartmental pressures on exertion in a patient with a popliteal artery
entrapment syndrome, Am. J. Sp. Med., 13, 365, 1985.
82. Allen, M.J., Barnes, M.R., Bell, P.R.F., Bolia, A., and Hartshorne, T.C., Popliteal
entrapment syndrome: misdiagnosed as a compartment sydnrome, Eur. J. Vasc. Surg.,
7, 342, 1993.
83. Lysens, R.L., Renson, L.M., Ostyn, M.S., and Stalpaert, G., Intermittent claudication
in young athletes: popliteal artery entrapment syndrome, Am. J. Sp. Med., 11, 177,
1983.
84. Stipa, S., Cavallaro, A. and Marzo, L.d., Popliteal artery entrapment syndrome, Curr.
Surg. Ther., 3, 578, 1989.
85. Represa, J.A.F., Diego, J.A.D., Molina, L.M., Delgado, I., Calvo, M.G., Canizo, J.F.
et al., Popliteal artery entrapment syndrome, J. Cardiovasc. Surg., 27, 426430, 1986.
86. Ikeda, M., Iwase, T., Ashida, K., and Tankawa, H., Popliteal artery entrapment
syndrome: report of a case and study of 18 cases in Japan, Am. J. Surg., 141, 726, 1981.
87. Sammarco, G.J., Russo-Alesi, F.G., and Munda, R., Partial vascular occlusion causing
pseudocompartment syndrome of the leg: a case report, Am. J. Sp. Med., 25, 409,
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88. Marzo, L.d., Cavallaro, A., Sciacca, V., Mingoli, A., and Tamburelli, A. Surgical
treatment of popliteal artery entrapment syndrome: a ten-tear experience, Eur. J. Vasc.
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89. Iida, T. and Kobayashi, M., Tibial nerve entrapment at the tendinous arch of the
soleus: a case report, Clin. Orthop., 334, 265, 1997.
90. Ekelund, A.L., Bilateral nerve entrapment in the popliteal space, Am. J. Sp. Med., 18,
108, 1990.
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91. Sammarco, G.J. and Conti, S.F., Anomalous tibial nerve, Clin. Orthop. Rel. Res., 305,
239, 1994.
92. Podore, P.C., Popliteal entrapment syndrome: a report of tibial nerve entrapment, J.
Vasc. Surg., 2, 335, 1985.
93. Mozes, M., Ouakine, G., and Nathan, H., Saphenous nerve entrapment simulating
vascular disorder, Surgery, 77, 299, 1975.
94. Luerssen, T.G., Campbell, R.L., Defalque, R.J., and Worth, R.M., Spontaneous saphenous neuralgia, Neurosurgery, 13, 238, 1983.
95. Romanoff, M.E., Cory, P.C., Kalenak, A., Keyser, G.C. and Marshall, W.K., Saphenus
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97. Hemler, D.E., Ward, W.K., Karstetter, K.W., and Bryant, P.M., Saphenous nerve
entrapment caused by pes anserinus bursitis mimicking stress fracture of the tibia,
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98. Ochoa, J.L. and Torebjrk, H.E., Paraesthesiae from ectopic impulse generation in
human sensory nerves, Brain, 77, 835, 1980.
99. Schon, L.C., Nerve entrapment, neuropathy, and nerve dysfunction in athletes,
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101. Reisin, R., Pardal, A., Ruggieri, V., and Gold, L., Sural neuropathy due to external
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105. Gardner, A.M.N., Fox, R.H., Lawrence, C., Bunker, T.D., Ling, R.S.M., and
MacEachern, A.G., Reduction of post-traumatic swelling and compartment pressure
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290, 1273, 1985.
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111. Gerkin, T.M., Beebe, H.G., Williams, D.M., Bloom, J.R., and Wakeld, T.W.,
Popliteal vein entrapment presenting as deep venous thrombosis and chronic venous
insufciency, J. Vasc. Surg., 18, 760, 1993.
15
Composition and
Function of the
Interstitial Space
INTRODUCTION
The interstitial space includes the connective tissues that intervene among cells,
blood capillaries, and lymph vessels. The volume of the space is about 15% of body
weight.1 It is also an extravascular fluid system that is generated by capillary filtration
(Figure 15.1). The extravascular flow system functions to support the tissues metabolic demands and to maintain an optimal and stable environment for the cells.
This is the space in which hydrostatic pressures are measured for clinical purposes
and for research to determine limits for tissue nutrition and viability.
MUSCLE
AND
TENDON
Skeletal muscles comprise approximately 40% of the body weight. The volume of
interstitial space varies among tissues. It is 5% of the muscle tissue volume whereas
it is 95% of the volume in the tendon. Muscles may increase metabolism 50-fold.
Muscle tissue may increase blood flow 100-fold during activity compared to at rest.
Skeletal muscle is the engine of locomotion, posture, and respiration. Muscular
tension increases the strength of the long bones of our limbs by pretentioning.
Skeletal muscle protects the viscera, participates in heat production, and is storage
for many important nutrients, electrolytes, and divalent ions.
Normal function of muscle tissue requires normal function of muscle fibers,
nerve, vasculature, and tendon. The study of these functions is labeled muscle
physiology. Normal function of muscle tissue also requires a mechanical load.
Muscular biomechanics is the study of the response of the muscle to mechanical
loading. Therefore, muscular biomechanics is the study of how force is transferred
from muscle fiber through the interstitial space to the tendon and its insertion. It
also includes studies on muscular geometry, muscular stress, and intramuscular
pressure generation.
COMPOSITION OF THE INTERSTITIAL SPACE

The interstitial space is composed of a framework of fibers (matrix) and an amorphous mucopolysaccharide gel (Figure 15.2). The fibers may extend long distances
through the interstitium. They are strong and carry most of the compressive and
tensile forces of the interstitial space of all tissues. The fibers may be collagenous,
221
222
Capillary
Pv
Pa
Intravascular
Lymph vessel
Interstitial
Fluid flow
Prelymphatic space
Intracellular
Cell
FIGURE 15.1 Schematic illustration of tissue spaces. The fluid flow to and through the
interstitial space is indicated by solid arrows.
reticular, or elastic. They are synthesized by mesenchymal cells and fibroblasts.

Molecular collagen is secreted from the cells into the interstitial ground substance,
where it is polymerized to collagenous and reticular fibers.2 The gel consists of two
interpenetrated phases, one a solid-like phase arranged in the form of a network
whose strands are linked together. The solid-like phase consists of thin, coiled
proteoglycan filaments. They look like brushes and are composed of 98% hyaluronic
acid and 2% protein. The second phase is the space between the solid filaments,
which is filled with entrapped fluid. The gel is thus a conglomerate of small filaments
of small proteoglycan and hyaluronic acid fibers in which most of the water is
entrapped (Figure 15.3). This prevents, or at least resists, fluid shift from upper parts
to dependent parts of the body. An additional function of the gel is to keep adjacent
cells partially separated from each other.3 The interstitial space also contains non-
Interstitial space
Matrix
Gel
Solid
Fluid
FIGURE 15.2 The interstitial gel is composed of solid components with entrapped fluid.
Composition and Function of the Interstitial Space
223
Proteoglycans
Canaliculi
Free fluid
Collagen fibers
Cell
FIGURE 15.3 Components of the interstitial space. The background represents the gel and
interstitial fluid.
endothelialized microscopic channels ending in the prelymphatic space.4 They are

particularly important in regions where there are no lymphatic vessels.
The extracellular matrix of muscle consists of laminid, fibronectin, entactin,
and collagen. It is organized into three interconnected sheaths. A collagenous epimysium surrounds the whole muscle. Collagen fibers extend inward from the epimysium
to form the perimysium. Nerve branches, blood vessels, muscle spindles, and fat
cells lie within the perimysium. Individual muscle fibers are covered with a sheath
of endomysium. The endomysium contains capillaries, fine nerve branches, fibroblasts, macrophages, and a network of extracellular fibrils. The basal lamina is the
endomysial component that lies closest to the muscle fiber surface. Satellite cells
are wedged between muscle fiber and basal lamina.
FUNCTION OF THE INTERSTITIAL SPACE

The location of the interstitial space reflects the different functions it serves. The
interstitial space is an extravascular flow system and a fluid reservoir. It has a storage
function and gives immunological support. The solid structures of matrix give elastic
support and participate in force transmission.
EXTRAVASCULAR FLOW SYSTEM

As a gel interposed between the capillary and lymphatic barriers, the interstitial
space exerts influence on transcapillary partition and exchange of water and large
solutes between blood and lymph. The interstitial fluid hydrostatic pressure determines the magnitude and direction of the fluid flow. The fluid flow system is a
transport medium for nutrients and waste products.
224
Large molecules are transported through interstitial channels that end in endothelial-lined sacs that convert to collecting lymph channels.5 The channels, which
are widened by edema, facilitate convective flow.
In normally hydrated tissue, the interstitial space is a barrier against macromolecular transport. The structure of the interstitial space prevents flow of interstitial
fluid from one level of the body to another. This preventive mechanism is disregarded
in clinical conditions with edema. The change of hydraulic conductivity through the
interstitial space in edematous tissue results in fluid flow to dependent parts of the
extremity. On the other hand, fluid flow by convection is superimposed on many
diffusion processes. This kind of flow is a prerequisite for transportation of large
molecules such as hormones, enzymes, inhibitors, and activators.
FLUID RESERVOIR
The interstitial fluid space, which is three times larger than the intravascular space,
also serves as a fluid reservoir for the cardiovascular system. An alteration in
circulating plasma volume elicits a fluid shift across the capillary wall to maintain
normal vascular filling.1 The interstitial space consumes large volumes of fluid from
the intravascular space during limb swelling. This may occur during a reperfusion
syndrome69 or following longstanding external compression, resulting in a crush
syndrome.1013 Large volumes from the intravascular space may be withdrawn,
leading to hypovolemic shock. The space is a continuous fluid reservoir that provides
a pathway for diffusion and convection.
STORAGE FUNCTIONS
As an ion-exchange resin, the matrix serves as a site for storage of large quantities of
electrolytes, especially Na+ and Ca2+. It is an important reservoir of water and lipids.
IMMUNOLOGICAL SUPPORT
Many immunological reactions occur in this space. The channels of the space
facilitate the communication and control of the defense mechanisms. The space acts
as a barrier against infections and transportation of large molecules.
ELASTIC SUPPORT
The solid structures of the matrix provide elastic support and shock absorption for
all cells. They can withstand longstanding and high pressures to resist tensile,
compressive, and shear mechanical stresses, especially in bone and cartilage tissue.
In bone tissue, most of the interstitial tissue is mineralized. In myocitis ossificans,
the muscle tissue is calcified.
REGENERATION
OF
MUSCLE TISSUE
The interstitial space serves as a scaffold for muscular generation following muscular
damage due to ischemic, thermal, and mechanical insult. New muscle fibers regenerate from a resident population of satellite cells, which are wedged under the
225
endomysium of muscle fibers.1416 The numbers of nuclei of the satellite cells are
about 5% of the muscle nuclei. The basal lamina of nerves and blood vessels also
acts as a scaffold for generation. If the basal lamina is preserved, myotubes form
within the original sheaths. If the myotubes are not oriented in parallel, the regenerated muscle generates less tensile force.
FORCE TRANSMISSION
Components of the extracellular matrix contribute to the mechanical properties of
muscle. They serve to bind the contractile units together to provide for integrated
motion among the muscle fibers during contraction. Longitudinal tension is required
to restore the normal anatomy of the internal fibrous tissue of regenerating muscle
tissue.14 It is a prerequisite to regain normal muscle function.
The interstitial space accounts for the tensile strength of muscle, the distribution
of force within muscle and the transmission of force from muscle to tendon. The
contractile entity of muscle fibers is the sarcomere. The basal lamina takes part in the
distribution of force along the muscle fiber as well as in the transmission of force from
muscle to tendon. Molecules that connect basal lamina to muscle plasma membrane
along its length and at the myotendinous junction provide possible basis for this mechanical linkage.17 Muscle fibers are bound together by the matrix of the interstitial space
into contractile units, which provide integrated motion stimulation. During muscle
contraction, these filaments transfer tensile force generated by the muscle fiber to the
interstitial space and further to the tendon. In this respect, the tendon can be regarded
as a continuous extension of the interstitial space of the muscle itself (Figure 15.4).
Tendons transmit the forces generated by muscles to bone. The primary function
is to achieve movement and stability of the body. The digital flexor and extensor
tendons are stiff, whereas the Achilles tendon is more elastic and may be stretched
in late stance phase. Tendons store energy on stretching and release it when the
muscle contracts again.
NEUROMUSCULAR TRANSMISSION
The structure and function of the extracellular matrix are specialized at site for
neuromuscular transmission. Acetylcholine transmits the nerve signal to the muscle.
It is hydrolyzed by acetylcholinesterase, which is the only enzyme known to be
associated in the extracellular space.
BIOMECHANICS OF THE INTERSTITIAL SPACE

Mechanical forces alter tissue growth and remodeling. The relationship is well
documented and described in Wolfs law.18 One mechanism for this may be convection, which alters the mRNA synthesis. The solid network can carry shear stresses
for an indefinite period of time. A force applied to one face of the matrix exerts
compressive stresses or tensile stresses in the collagen fibers throughout the matrix.
The matrix allows the interstitium to become mechanically deformed and to return
to the initial state (Figure 15.5).
226
FIGURE 15.4 Relation among muscle fibers, the interstitial space, and the tendon. Tensile
forces are transmitted along the whole muscle fiber by filaments into the interstitial space,
which extends into the tendon.
Pcollagen
Pext.
IIgel
A.
B.
FIGURE 15.5 External forces (Pext), the tensile forces of the collagen fibers (Pcollagen) and the
swelling pressure of the interstitial gel (gel) create the mechanical equilibrium of the interstitial
space. Solid components (A) such as collagen are under tension, whereas the gel (B) exerts
a swelling pressure.
FORCES
AND
227
STRESSES
A fluid deforms continuously under shear stress. Two kinds of forces act on fluids:
(1) gravity and electrostatic forces act without physical contact; (2) compressive
forces (pressure) and frictional forces require contact for transmission. These forces
are called surface forces because they require a surface for their action. Stress created
by gravity is a vector. It is a surface force per unit area. Stress is a vector because
it has a magnitude and a direction (tensor of the second order). Fluid pressure, on
the other hand, has only a magnitude and is therefore a scalar.
Shear stresses can only survive in the matrix network where they can deform
the structure. In the fluid phase, shear stresses fall to zero because of fluid flow. The
interstitial gel has been suggested to have characteristics between a solid and a fluid.
Therefore, transmission of pressure through a gel obeys laws of pressure transmission that are a combination of both fluid and solid fiber pressure transmissions.3
In normally hydrated muscle and subcutaneous tissue, 50 to 100% of the force
applied by external compression is transmitted into the fluid phase.1923 In normally
hydrated tissue, 60 to 70% of the applied pressure is transmitted,22 whereas in
edematous tissue 100% of the pressure is transmitted.22 This is also true for transmission of subatmospheric pressures.24
HYDROSTATIC PRESSURE GENERATION

Muscle fibers shorten 20% during maximal contraction. During contraction, the
radius of the fiber curvature decreases by 50%. By using different mechanical
models on muscular geometry, it is possible to explain by using the law of Laplace
why intramuscular pressure is higher in the central part of the muscle.2527 Also,
by applying the law of Laplace to a muscle with curved fibers and to a muscle
with straight fibers, it is possible to explain why a curved muscle fiber with short
radius of the fiber curvature generates higher stress to the muscle compared with
that by a straight muscle fiber with a longer radius of fiber curvature. The
relatively high stresses in the curved fiber generate high intramuscular pressures,
as seen at the end of concentric muscular activity (Figure 15.6).28 If the thickness
of the fiber is h, and the number of fibers is n, the intramuscular pressure p can
be calculated as:
p = po + s nh/r
(15.1)
where po is the hydrostatic pressure beneath the fascia, r is the radius of the fiber
curvature, and s is the stress in each fiber.2527 The value of snh/r, i.e., the hydrostatic
pressure, increases as the r value decreases.
AS A
MEASURE
OF
FORCE GENERATION
Muscle contraction pressure is the interstitial fluid pressure created by a muscle

as it contracts within its fascial compartment. This pressure correlates linearly
with a contraction force in a specific muscle during isometric exercise of a wide
range of forces.
228
Curved fibers:
h
Short radius (r)
Straight fibers:
h
Long radius (R)
FIGURE 15.6 Different curvatures of muscle fibers with different lengths of the radius of
the curvature. The number (n) and thickness (h) of fibers and the radius (R) of the fiber
curvature determine the magnitude of the hydrostatic pressure.
Currently, there are no direct practical methods for measuring force production of
individual muscles during dynamic exercise in humans. Implantation of a buckle transducer on a tendon is the most direct technique for individual muscle force assessment.29
PRESSURES
IN THE INTERSTITIAL
SPACE
Starling described the different pressures responsible for fluid shift between the
capillaries and the interstitial space.30 Scholander31 and Wiederhielm32 described the
concept of a subatmospheric interstitial fluid pressure and physiochemical nature of
the interstitium.
Following the structures in Figure 15.2, there are two kinds of tissue pressures
in the interstitial space: (1) interstitial hydrostatic pressure, which is a scalar, and
(2) interstitial solid tissue pressures, which are vectors. Total tissue pressure has
been suggested to be the algebraic summation of the fluid and solid tissue pressure.3
However, this concept is controversial, because a scalar and a vector must not be
added. Hydrostatic pressures and forces in solid structures may be mechanically
linked. They may balance forces in the solid structures of the interstitial space.
Mechanical deformation of solid structures influences the hydrostatic pressure
because the resistance for fluid flow through the normally hydrated interstitial space
is normally high. This means that the hydraulic conductivity is fairly low.
INTERSTITIAL FLUID PRESSURES

The interstitial fluid hydrostatic pressure is transmitted in the tissue by fluid. In a
normally hydrated tissue, most of the fluid is bound in the gel phase. Free fluid
exists only in the canaliculi, which end up in the prelymphatic space.4
229
Starling, in 1896, described the regulation of fluid across capillary walls in what
we presently call the StarlingLandis equation,30 which was later modified by also
taking the Staverman reflection coefficient for total protein into account:
Jc = Kf [(Pc Pt) b(pc pt)]
(15.2)
where Jc is the net fluid flow across the capillary wall, Kf the capillary filtration
coefficient, Pc the capillary blood hydrostatic pressure, Pt the hydrostatic pressure in
the interstitial fluid, b the capillary membrane reflection coefficient, pc the capillary
blood colloid-osmotic pressure, and pt the osmotic pressure in the interstitial fluid.
The interstitial fluid hydrostatic pressure (Pt) has a strategic position between
the capillaries, cells, and lymphatics. It determines the magnitude and the direction
of fluid movement between capillaries, cells, and lymphatics (Figure 15.1). It also
determines whether free interstitial fluid will move in or out of the interstitial gel.
Interstitial fluid pressure together with intracellular osmotic and hydrostatic pressures determines fluid flow through cell membranes. If the capillary filtration and
the reflection coefficients are disregarded in Equation 15.1, the interstitial fluid
pressure may be expressed as:
Pt = Pc (pc pt)
(15.3)
This implies that the negative free fluid pressure in the interstitium is in equilibrium
with and equal to the absorption pressure of the interstitial gel, but not caused by it.3
SOLID TISSUE PRESSURE

Solid tissue pressures are pressures transmitted by the solid components. They are
caused by forces that deform solid tissue structures. These types of pressures are
never evenly distributed. Pressures within solids are rather stresses. Both pressures
and stresses are subject to the same unit of measurement, namely force per unit area
(Pascal or mmHg). Stresses vary throughout a solid body. Therefore, it is not possible
to assign a single stress value to the interstitial fibers.
TOTAL TISSUE PRESSURE

Tissue pressure may also be involved in the forces from solid components operating
on a vessel wall. The sum of hydrostatic and solid pressures is defined as total tissue
pressure. This may be illustrated by the law of Laplace:
Pi Po = T/R
(15.4)
where Pi is the intravascular hydrostatic pressure and Po the sum of all extravascular
pressures. The equilibrium between these two pressures are balanced by the tension
in the vessel wall (Twall) and the radius of the vessel (R). Po is the summation of all
the partial pressures exerted on a collapsible vessel wall by cells, fluids, matrix, and
the gel wall.3,33 In Figure 15.7, the summation of all extravascular pressures is labeled
Ptotal. It cannot be assumed that Pt in Equation 15.3 is equal to Po in Equation 15.4,
230
Pcell
Pgel
Twall
Pmatrix
Pc
Pt
Ptotal
Pc Ptotal = Twall/ R
FIGURE 15.7 The total tissue pressure (Ptotal) is the sum of all the partial pressures from the
cells, the interstitial gel, the matrix, and the interstitial hydrostatic pressure. The difference
between the capillary pressure (Pc) and total tissue pressure is equal to the tension (T) in the
wall divided by the radius (R) of the vessel.
or Ptotal in Figure 15.7. The difference between the Pc value and Ptotal value is the
transmural pressure gradient. If Po increases to abnormal levels, it may affect the
local blood flow through the tissue.
The concept of total tissue pressure is controversial. The total pressure exerted
on any given surface area in the tissue is defined as total tissue pressure. The total
tissue pressure tends to compress blood vessels and other intratissue structures.3,32
Total tissue pressure is not possible to measure, but it may be reflected by increased
interstitial fluid hydrostatic pressure,34 because different tissues have different
abilities to withstand external forces. External forces may be transmitted into the
tissue by both hydrostatic pressure and by compressive and tensile forces. The
capacity of the solid components to withstand deformation as a response to external
compression will decide the magnitude of tissue hydrostatic pressure. The effects
of external compression on interstitial fluid pressure and solid tissue pressure was
studied by Brace and Guyton.19 They showed that the interstitial fluid hydrostatic
pressure changed by 70% of the applied pressure in a normally hydrated tissue.
In an edematous tissue, the fluid pressure changed by 100% of the applied pressure.19,22 In overhydrated tissue, the interstitial fluid pressure was equal to total
tissue pressure (Figure 15.8). External compression induces a blood volume shift.
If the volume shift is impeded, the interstitial pressure changes by 100% of the
applied pressure. The interstitial hydrostatic pressure may be considered the
mechanical resultant of the interaction between hydrostatic and osmotic pressures
on the one hand and mechanical forces on the other.
COMPLIANCE OF THE INTERSTITIAL SPACE

Interstitial compliance (C) is defined as the ratio between changes in the interstitial
fluid volume (DV) and the interstitial fluid pressure (DP):
231
Ptotal
IIgel
Psolid
Phydrostatic
FIGURE 15.8 Total tissue pressure as the summation of pressure exerted by solid and fluid
components of the tissue.
C = DV/DP
(15.5)
A low compliance implies that a small rise in interstitial fluid volume causes a large
rise in interstitial fluid pressure. The compliance of a dehydrated tissue is low (Figure
15.9). Once the interstitial fluid pressure reaches atmospheric pressure level, the
compliance suddenly increases manifold.3 Substantial amounts of free fluid may be
accumulated in the tissue with only minor pressure increase. Free fluid is the mobile
fluid within the space. Pumping of the lymphatic system is the basic cause of the
negative pressure in the interstitial space.35 Taylor et al. showed that lymph flow
increased up to 50-fold when interstitial fluid pressure increased from 6 mmHg to
atmospheric level.36
Compliance of normally hydrated muscle tissue is high at rest.37 The volume
of muscle tissue may increase up to 20% following heavy exercise. In this situation,
after activity the compliance decreases. Amplitudes of the pulssynchronous intraTissue pressure
C.
Positive
100%
B.
Volume %
Negative
A.
Low compliance
High compliance
Low compliance
Hydraulic
resistance
?
Volume %
FIGURE 15.9 Relationship among tissue pressure, tissue volume, and hydraulic resistance
in the tissue during different degrees of hydration. The compliance of edematous tissue is
high (B). In dehydrated tissue (A) and in tissues with abnormal swelling (C), the compliance
is low. The hydraulic resistance decreases once the tissue is edematous.
232
muscular pressure oscillations have been measured in normally hydrated muscle as

well as following maximal exercise in normal subjects and in patients with chronic
compartment syndrome. Patients with chronic compartment syndromes have significantly larger amplitude of the pulssynchronous intramuscular pressure oscillations
after exercise as a sign of decreased compliance.
HYDRAULIC PERMEABILITY
OF THE INTERSTITIAL SPACE
Glycosaminoglycans of the interstitial space have at physiological pH a net negative
charge and are osmotically active. Therefore, they restrict free diffusion through the
interstitium. The resistance to fluid flow through the interstitial canaliculi increases
with 1/r4. It is high in a normally hydrated interstitial space (Figure 15.9).
Hydraulic permeability is the ability of water to flow through a tissue. The interstitial space contains interconnecting water-filled pores through which water flows. The
flow rate is directly proportional to the pressure gradient over the tissue segment and
to the cross sectional area. The hydraulic permeability can be described by Darcys law:
Q = k Ad P/x
(15.6)
where Q is the flow rate (ml/min), k the hydraulic permeability, A the cross sectional
area, dP/x is the pressure gradient across the tissue segment. The hydraulic permeability (k) varies with the degree of tissue hydration. In edematous tissue, the
hydraulic permeability is high. Water flows easily through the tissue because the
resistance for fluid flow is low. In dehydrated tissues, the k value is low, i.e., the
resistance for fluid flow is high.
Inflammatory reactions increase vascular permeability34,38,39 and cause a disaggregation of the ground substance. These changes favor activation and movement
of fixed tissue macrophages as well as migration of inflammatory cells such as
monocytes, leukocytes, and lymphocytes into the interstitial space. The increased
movement of these cells contributes to increased immunological defense of the body.
SUMMARY
The volume of the interstitial space is 15% of the body weight, which is about three
times more than that of the intravascular space. The volume of the interstitial space
varies among tissues. It is 5% of the muscle tissue volume and 95% of the volume
in the tendon. The interstitial space is an extravascular fluid system that supports
the metabolic demands and acts as a fluid reservoir. It has a storage function and
gives immunological support. Solid structures of matrix give elastic support and
participate in muscular force transmission. The interstitial fluid hydrostatic pressure
determines the magnitude and direction of fluid flow among capillaries, cells, and
lymphatic vessels. Pumping of the lymphatic system is the basic cause of the negative
pressure in the interstitial space. The interstitial hydrostatic pressure may be considered the result of the interaction between hydrostatic and osmotic pressures on
233
the one hand and mechanical forces on the other. Patients with chronic compartment
syndromes have significantly larger amplitude of the pulssynchronous intramuscular
pressure oscillations after exercise as a sign of decreased compliance of the interstitial space.
REFERENCES
2. Haljame, H., Anatomy of the interstitial tissue, Lymphology, 11, 128, 1978.
3. Guyton, A.C., Granger, H.J., and Taylor, A.E., Interstitial fluid pressure, Physiol. Rev.,
51, 527, 1971.
4. Casley-Smith, J.R., Channels through the interstitial tissue, Bibl. Anat., 15, 206, 1977.
5. Zweifach, B.W. and Silberberg, A., The interstitial lymphatic flow system, in Cardiovascular Physiology III, Guyton, A.C. and Young, D.B., Ed., University Press,
Baltimore, 1979, chap. 18, p. 215.
8. Menger, M.D., Barker, J.H., and Messmer, K., Capillary blood perfusion during
postischemic reperfusion in striated muscle, Plast. Reconstr. Surg., 89, 1104, 1992.
853, 1988.
10. Mubarak, S. and Owen, C.A., Compartment syndrome and its relation to the Crush
12. Rommel, F.M., Kabler, R.L. and Mowad, J.J., The crush syndrome: a complication
of urological surgery, J. Urol., 135, 809, 1986.
13. Taylor, D.C., Salvian, A.J., and Chackleton, C.R., Crush syndrome complicating
pneumatic antishock garment (PASG) use, Br. J. Accid. Surg., 19, 43, 1988.
14. Allbrook, D., Skeletal muscle regeneration, Musc. Nerve, 4, 234, 1981.
15. Bischoff, R., Regeneration of single skeletal muscle fibers in vitro, Anat. Rec., 182,
215, 1975.
Physiol. Scand., 135, 537, 1989.
17. Tidball, J.G. and Chan, M., Adhesive strength of single muscle cells to basement
membrane at myotendinous junction, J. Appl. Physiol., 67, 1063, 1989.
18. Wolff, J., Das Gesets der Transformation der Knochen, Hirschwald, Berlin, 1892.
19. Brace, R.A. and Guyton, A.C., Transmission of applied pressure through tissues:
interstitial fluid pressure, solid tissue pressure and total tissue pressure, Proc. Soc.
Exp. Biol. Med., 154, 164, 1977.
J. Orthop. Res., 11, 818, 1993.
234
22. Reddy, N.P., Palmieri, V., and Cochran, G.V.B., Subcutaneous interstitial fluid pressure during external loading, Am. J. Physiol., 240, R327, 1981.
23. Thomson, A.E. and Doupe, J., Some factors affecting the auscultatory measurement
of arterial blood pressures, Can. J. Res., Sect. E, 27, 72, 1949.
24. Crenshaw, A.G., Wiger, P., and Styf, J., Evaluation of techniques for measuring
negative intramuscular pressures in humans, Eur. J. Appl. Physiol., 77, 44, 1998.
26. Skalak, R., Approximate formulas for myocardial fiber stresses, Trans. ASME, 104,
162, 1982.
27. Styf, J., Ballard, R., Crenshaw, A., Watenpaugh, D., and Hargens, A.H., Intramuscular
pressure and torque during isometric, concentric and eccentric muscular activity,
Scand. J. Sci. Sp., 5, 291, 1995.
29. Komi, P.V., Stretch-shortening cycle: a powerful model to study normal and fatigued
muscle, J. Biomech., 33, 1197, 2000.
30. Starling, E.H., On the absorption of fluids from the connective tissue spaces, J.
Physiol. (Lond.), 19, 313, 1896.
fluid of animals, Science, 161, 321, 1968.
32. Wiederhielm, C.A. and Weston, B.V., Microvascular lymphatic and tissue pressures
in the unanesthetized mammal, Am. J. Physiol., 225, 992, 1973.
1979.
34. Brace, R.A., Progress toward resolving the controversy of positive vs. negative interstitial fluid pressure, Circ. Res., 49, 281, 1981.
35. Taylor, A.E., Gibson, W.H., Granger, H.J., and Guyton, A.C., The interaction between
intracapillary and tissue forces in the overall regulation of interstitial fluid volume,
Lymphology, 6, 192, 1973.
36. Taylor, A.E., Capillary fluid filtration: Straling forces and lymph flow, Circ. Res., 49,
557, 1981.
characteristics of the interstitial fluid space in the skeletal muscle of the cat, Acta
Physiol. Scand., 90, 583, 1974.
38. Aukland, K., Fadnes, H.O., Noddeland, H., and Reed, R.K., Edema preventing mechanisms in subcutis and skeletal muscle, in Tissue Fluid Pressure and Composition,
Hargens, A., Ed., Williams & Wilkins, Baltimore, 1981.
Scand., 104, 318, 1978.
16
Measurement of
Intramuscular
Pressures at Rest
INTRODUCTION
Accurate measurement of hydrostatic pressure is a valuable tool in the diagnosis of

acute15 and chronic compartment syndromes.613 This measurement has been used
to study the interstitial space14,15 and uid shift over the capillary bed.16 The interstitial uid hydrostatic pressure is one of the Starling forces that affects uid transportation over the capillary bed.17 It is an additional important parameter in physiological studies of tissue nutrition and viability.18
This chapter discusses the difculties associated with invasive measurements
of static intramuscular pressure at rest. Static pressure in muscle tissue is rather
quasi-static, because it varies slowly, with a time constant of several seconds or
minutes. The difculties to be considered during intramuscular pressure recordings
include trauma to muscular tissue by the recording device and occlusion of the
catheter or needle especially during measurements for an extended period of time.
Attention should also be paid to how muscle tissue is affected by the volume load
following injection or infusion. The contact areas between the pressure-recording
catheter and the tissue as well as the static properties of the pressure-recording
equipment are important issues. Finally, measurement of intramuscular pressure,
including technical knowledge and how to handle the technique for catheter insertion,
has a signicant learning curve.
MEASUREMENT QUALITY
A sensor converts a physical measurand, in this case a hydrostatic pressure, to a
manageable quantity, e.g., an electrical signal. Important features of a pressure
transducer that should be tested are accuracy, sensitivity, linearity, and hysteresis,
all of which are discussed next.
ACCURACY
Static accuracy is the reliability of the device to record stationary slow variations
of intramuscular pressure. To obtain static accuracy, the system must be stable with
a nondrifting baseline. If the recording system is not stable enough, it needs frequent
baseline and calibration checks. The ability to determine the exact pressure and to
reproduce a measurement achieving the same result is a desirable quality of a
235
236
transducer. Temperature drift is a common problem. Noise is unpredictable uctuations of the output. It can be reduced by several ltering techniques.
SENSITIVITY
Sensitivity of a device is its ability to produce an output signal as a reaction of the
pressure input. Static sensitivity of a transducer is the relation between an input (x)
and output (y) signal. The sensitivity (s) of a transducer is dened as:
s = Dy/Dx
(16.1)
where Dy is the output change due to the input change Dx. The performance of the
pressure-recording system may be tested by measuring the applied pressure and the
recorded pressure at a low frequency. This may be regarded as a static calibration.
The slope of the curve in Figure 16.1 illustrates the concept of sensitivity (s). A
static pressure calibration curve should be linear to allow for a good sensitivity.
Furthermore, the curve should maintain at origo (0,0). Environmental factors such
as temperature and exposure to vibrations may change the sensitivity, and the curve
may drift from origo. This is called a zero drift. Transducer-tipped catheters may
be sensitive to temperature drift. The drift (mmHg/C) must be known. Figure 16.1
illustrates sensitivity drift as well as zero drift. Fluid-lled pressure-recording systems may be repeatedly calibrated for zero drift. Bavetta et al. reported that zero
Voltage (y)
B.
A.
y
x
Hydrostatic pressure (x)
Sensitivity: y/x
FIGURE 16.1 Linearity, sensitivity, and zero drift. The applied pressure is on the x-axis. The
output is measured as voltage and plotted on the y-axis. Sensitivity is calculated from the
calibration curve (A) by the slope of the least-squares line (dotted) which runs through origo.
Curve B illustrates a zero drift (arrow).
Measurement of Intramuscular Pressures at Rest
237
Voltage (y)
Hydrostatic pressure (x)
FIGURE 16.2 Hysteresis of a pressure curve. The pressure curves behave differently during
pressurization and unloading. Hysteresis may be caused by both electrical and mechanical reasons.
drift of ber-optic pressure transducers was a signicant problem.19 These catheters

cannot easily be recalibrated following insertion.
LINEARITY, UNIQUENESS,
AND
HYSTERESIS
Linearity is a quality of the sensor which roughly means that changing input pressure
by a certain factor will result in a change of the output with the same factor (Figure
16.1). If the transducer response is linear, the sensitivity is constant all over the
range of the transducer.
The system must imply uniqueness, which means that it will respond uniquely
to any statically applied signal regardless of the way the signal is applied. Hysteresis
exhibited by some recording systems is an example of lack of uniqueness in static
response. Hysteresis of a pressure curve describes the behavior during pressurization
and unloading (Figure 16.2). It may be due to electrical and mechanical components.
It may result from energy being absorbed by the system during pressurization and
being recovered during decompression (Figure 16.2).
COMPLIANCE OF THE PRESSURE-RECORDING

SYSTEM
It is important to know the compliance of the pressure-recording system. Pressure
changes will be erroneous if the volume shift at the tip of the catheter is too small
to have a complete effect on the transducer. The compliance (C) of a transducer is
the relation between the volume change (DV) and the pressure change (DP), given
by the following equation:
C = DV/DP
(16.2)
238
A crucial and maybe the most difcult part of the preparation for pressure recordings
is lling the transducer and the transducer line with saline that is free of entrapped
air bubbles. Even ne air bubbles in the recording system increase the total compliance considerably and decrease the dynamic properties. If cold saline from the
refrigerator is used, air bubble formation increases at room temperature. The same
is true when saline at room temperature in the catheter is exposed to warm (35 to
38C) skin and muscle tissue. Compliance of uid-lled pressure transducer plus
catheter ranges between 0.089 and 0.14 mL/mmHg.10,2022
CATHETER INSERTION TECHNIQUE

Calibration and check of all equipment must be done before the catheters are inserted.
The catheter insertion technique is important to obtain reliable intramuscular pressure
recordings. The best site for catheter insertion should be decided by palpating the
muscle belly during an active contraction and by using anatomical landmarks. Ca. 1
to 2 mL of local anesthesia should be installed subcutaneously. The underlying muscle
fascia should not be penetrated. Local anesthesia may inhibit local muscle function
and create a local swelling of the muscle by an inammatory reaction. The patient
should be asked to contract the muscle to be studied. For example, if the tibialis
anterior muscle is to be studied, the patient should dorsiex his/her ankle joint. The
introducer or troachar should be inserted through the skin and fascia with a sharp
steel needle while the patient keeps the muscle contracted (Figure 16.3A). The sharp
inner needle should be withdrawn slightly to a point where the plastic sheath of the
introducer (Figure 16.3B) protects the cutting edge of the needle tip.10 The patient
should be asked to relax his/her muscle. The plastic sheath should be inserted parallel
to the muscle bers simultaneously.23 The steel needle or troachar should be withdrawn (Figure 16.3C). No bleeding should be visible through the plastic sheath. If
this is the case, the investigation should be nished, the introducer retracted, a
compressive dressing applied, and the limb kept elevated for a short while.
The catheter should be connected to a transducer line lled with saline. The
catheter will be easily lled from a syringe at the transducer or from a saline bag
by ushing the microcapillary. The catheter should be inserted into the tissue through
the plastic sheath and the sheath retracted while keeping the catheter tip at the same
spot in the muscle (Figure 16.3D). The catheter should be secured to the skin.
Gelberman et al. described a volar approach starting at the junction of the
proximal and middle third of the forearm.24,25 McDoughall et al. suggested a dorsal
approach for catheter insertion in the supinated forearm.26 By using the ulna as a
guide, the catheter should be advanced through the dorsal compartment and
interosseous membrane into the deep volar compartment.
It is important that the catheter be inserted parallel with the muscle bers to
minimize trauma and discomfort.23 At least 2 cm of the catheter should be inserted
into the muscle to prevent uid leakage back along the catheter.22 This compares in
most cases at a total distance of 4 cm from the skin if the catheter is inserted parallel
with the muscle bers.23 An unintentional muscular activation may even be painful
if the catheter is placed in a wrong way. Chapter 17 discusses the matter more
extensively, and describes intramuscular pressure recordings during exercise.
239
(A)
(B)
(C)
(D)
FIGURE 16.3 Pictures of catheter insertion. After the muscle fascia has been penetrated,
the steel needle should be withdrawn a few millimeters into the plastic sheath of the
introducer (A). In this way the cutting tip of the needle will not traumatize the muscle
tissue when the introducer is advanced parallel with the muscle bers into the preferred
position (B). The steel needle is retracted (C) and replaced by the pressure-recording
catheter (D). Finally, the plastic sheath of the introducer is removed. (See color insert
RESPONSE
AND
LOCATION
OF THE
CATHETER TIP
Several tests are available to make sure that the tip of the catheter is located within
the muscle to be studied. The response of the catheter is checked by external
compression by a constant force over the muscle belly from distal to proximal by
the investigators ngertip. The pressure amplitude of the response is highest at
external compression over the catheter tip (Figure 16.4). Another catheter patency
test is intramuscular pressure recording during an active muscle contraction.27 As a
test of catheter location in the deep posterior compartment of the leg, intramuscular
pressure recordings during a maximum exion of the toes and then again during
plantar exion of the ankle joint are recommended (Figure 16.5). By analyzing the
pressure amplitude of the response by the two activities, the degree of agonistic
coactivation between the muscles may help to decide catheter location in the exor
digitorum muscle and posterior tibial muscle.28 Another way to determine catheter
location in the leg or forearm is ultrasound.29
TISSUE TRAUMA
DUE TO
CATHETER INSERTION
The extent of tissue trauma to the muscle depends on the technique for introducing
the catheter, the size of the introducer, and on the design of the catheter tip. The
240
Pressure
+1
+2
+3 Distance (cm)
FIGURE 16.4 Amplitude of intramuscular pressure oscillations, which is synchronous

with external compression by the investigators ngertip, is useful to identify location of
catheter tip. On the horizontal axis, 0 indicates the position of the catheter tip. The
distance distal (negative numbers) and proximal (positive numbers) from the catheter tip
are indicated.
5 seconds
Pressure
M. Flexor digitorum
Time
M. Tibialis posterior
Plantar flexion
of the ankle joint
Toe flexion
Time
FIGURE 16.5 Amplitude of intramuscular pressure in the exor digitorum longus muscle
(upper trace) and tibialis posterior muscle (lower trace) during exion of the ankle joint
followed by toe exion. The pressure responses indicate that catheters are correctly located.
The pressure response in the tibialis posterior muscle during toe exion is a sign of coactivation of the tibialis posterior muscle.
241
technique should be as atraumatic as possible. This can be achieved by choosing a

blunt insertion technique once the skin and the fascia have been penetrated, as shown
in Figure 16.3. By retracting the cutting needle into a position where the plastic tube
of the introducer covers the tip, the muscle bers are protected.10,30 As mentioned
previously, the catheter for intramuscular pressure measurements should be introduced parallel to the muscle bers (Figure 16.3).
When pressures are recorded by needle techniques, a separate cutting needle
may be used to penetrate the skin and subcutis. A semicutting needle with an
occluded tip and open sidehole(s) can be inserted through the holes and then
advanced into the muscle parallel with the bers.
Tissue injury at catheter insertion results in local inammation mediated by histamine, prostaglandins, and quinines.31 Tissue injury may increase capillary permeability and tissue swelling due to interstitial absorption of uid and proteins from the
vascular bed.32 This increases tissue uid hydrostatic pressure. The increased capillary
ltration due to increased permeability returns to normal values within 30 min. Therefore, intramuscular pressure decreases during the initial 30 min of pressure.
CATHETER OCCLUSION
Several principles have been used to prevent occlusion of the catheter tip by tissue
or by blood clots (Figure 16.6). The catheter tip can be closed and replaced by one
or several sideholes.22 Cotton or Dexon wicks that extend into the tissue from the
catheter may be used to prevent occlusion.33,34 Injection and infusion have been used
A.
B.
C.
D.
E.
FIGURE 16.6 Examples of different principles to prevent occlusion of the catheter tip. These
include multiple sideholes with (A) or without (B) an open tip, slits at the tip (C), and wick
strands (D) extending into the tissue. (E) The tip of the catheter may be covered by a protective
sheath, e.g., the STIC catheter.
242
to keep the tip open.10,22,3537 Protective sleeves around transducer-tipped catheters

have also been used.3840
CONTACT AREA
OF THE
CATHETER
The area of contact is the interface between the catheter tip and the surrounding
tissue over which hydrostatic pressure equilibration takes place. Many catheter tips
are designed to increase the contact area to obtain shorter equilibration time, prevent
occlusion, and decrease the risks of recording erroneously high pressure due to
volume load when catheters are infused or injected.
With the wick catheter method33,34 and the wick-in-needle method,41 the contact
area is increased by the strands of wettable material extending into the tissue from
the catheter or needle. The slit catheter has ve symmetrical slits at the end extending
3 mm along the length of the catheter tube.36
Teon catheters with multiple sideholes at their tip are another way of increasing the contact area.10,22,42,43 Needles for pressure recordings have also been
designed with one sidehole44 or several sideholes.43 Transducer-tipped catheters
may be combined with protective saline-lled sheaths with multiple sideholes.40
The sleeve also protects the transducer from forces exerted by solid components
in the tissues.
VOLUME LOAD
The volume load of muscle tissue during pressure recording depends on the volume
infused or injected during measurement and on the volume of the catheter itself.
High intramuscular pressures at rest have been reported with large catheters such
as the STIC catheter.45 This may be due to the sudden volume load by the catheter,
which is 2.5 mL combined with an infusion rate of 3 mL/h. Injection through
needles without sideholes may also give an erroneously high intramuscular pressure reading (Figure 16.7).43 When intramuscular pressures are recorded by the
injection techniques, one should wait for at least 30 sec following injection before
taking the pressure reading.
PHYSIOLOGIC REACTANCE
Physiologic reactance is the undesirable effect of any recording device on the
physiologic event. The concept has been emphasized in recordings of intraarterial
pressure46 and suggested to be valid for intramuscular pressure recording.47 The
presence of a catheter in muscle tissue may alter the function of the muscle because
of the discomfort or pain the subject may experience. Furthermore, most catheters
used in monitoring the interstitial uid hydrostatic pressure are at least 100 times
larger than the interstitial space itself. It is unlikely that under these conditions,
the uid hydrostatic pressure in the interstitial space behaves normally. Most
pressure-recording devices measure volume changes at the tip of the catheter. If
the device does not have a low compliance to the ow of uid in the interstitial
space, true pressures cannot be measured.
243
Pressure (mm Hg)
10 sec.
40
0
A.
B.
C.
D.
Time
FIGURE 16.7 Intramuscular pressure measured by the needle injection technique combined with an electrical transducer and recorder. (A) Intramuscular pressure at rest recorded
before injection. (B) Intramuscular pressure during injection. (C) Intramuscular pressure
following injection while the meniscus was concave. (D) Pressure recording when the
meniscus turned straight.43
CLASSIFICATION OF CATHETERS FOR

INTRAMUSCULAR PRESSURE MEASUREMENT
Direct pressure sensor systems can be divided into water-perfused systems and
catheter-tipped sensors. Fluid-lled systems are still the most common while the
new transducer-tipped systems are developing fast. To solve some of the problems
discussed previously, various catheters and methods for direct measurements of
pressure within muscle tissue have been devised. Techniques for intramuscular
pressure recordings can be classied based on the design of the catheter tip, location
of the transducer, and the medium through which the signal is transmitted.
DESIGN
OF THE
CATHETER TIP
Intramuscular pressure may be recorded by needles with different tip designs and
sizes, such as the wick catheter, wick-in-needle, Slit catheter, Intracath catheter,
and Myopress catheter (Figure 16.6). All these catheters require an extracorporal
transducer. The transducer must always be adjusted to the same height as the catheter
tip to avoid hydrostatic artifacts. Transducer-tipped catheters with or without a
protective sleeve need no height adjustment.
Needle Designs
The needle technique for recording tissue pressure was described in 1884.48 Since
then, the technique has been modied and applied to clinical use.35,37,49,50 In later
studies,37 the injected volume exceeds by far the 0.1 to 0.5 ml that was used in
earlier studies.35 Also, the design of the needle tip has been changed. To increase
the contact area, needles with multiple sideholes35,43,50 and with one sidehole and
a wick44 have been used. A needle without one or several sideholes at its tip is
244
less suitable for routine pressure measurements with the injection technique in the
clinical setting. However, measurements of intramuscular pressure with the meniscus method following injection and by a needle with multiple sideholes eliminate
the drawbacks mentioned.
Wick Catheter
Originally braided loose cotton wicks with a ber diameter of 8 to 16 mm were
pulled into the end of a Teon tubing by means of a monolament loop.34 The
tubing had an outer diameter of less than 1.5 mm. Its other end was connected to a
glass tube. The assembly was lled with saline to a given mark. The wick catheter
was inserted through a hypodermic needle, which was pulled back leaving the Teon
tubing with the wick in the tissue to be studied.
Mubarak et al. improved the wick catheter technique in 1976. They used soluble
braided No. 1 Dexon sutures with a ber diameter of 20 mm (Davis and Geck). Two
pieces, each 3.5-cm long, of the suture were tied at their midpoints to a 6-0 monolament suture which was 25 cm long.33 The lament was passed through an epidural
catheter with an outer diameter of 1 mm and an inner diameter of 0.6 mm. The lament
tted with a Luer-lock mount and a three-way stopcock. The Dexon bers were pulled
into the catheter for the distance of 1 cm, leaving 7.5 mm of the Dexon bers outside
the orice. The monolament was cut just inside the Luer-lock tting. In this way, the
wick bers were retrievable should they slip out of the catheter. Before insertion, the
catheter was connected to a transducer line and a transducer lled with sterile heparinized saline.33 It is important not to pack up the Dexon wicks too tightly into the
catheter orice to avoid partial occlusion. One piece of a shorter (2.5 to 3 cm) Dexon
also suits well. The wick catheter has no artifacts associated with uid injection. The
wick has an increased contact area with the tissue and keeps the orice of the catheter
open. However, the dynamic properties of the wick catheter are slow.10 It has been
suggested that the wick catheter measures osmotic pressure.51 In many studies, the
wick catheters are frequently ushed. In such cases, the device is no longer a noninfusion method, but rather an injection method.
Slit Catheter
The slit catheter consists of a 20-cm-long polyethylene tubing (PE 60). The tip of
the catheter has ve symmetrical slits that extend 3 mm along the length of the
tubing.36 The catheter is connected via a Luer-lock to a transducer line. The catheter
is gas-autoclaved in ethylene oxide. The whole pressure-recording system including
the catheter is lled with saline before insertion. The slits of the catheter prevent
occlusion of the tip and increase the contact area. The catheter has no detachable
pieces or parts. However, the slits may become distorted and occlude the tip of the
catheter if used during exercise.52
Myopress Catheter
The Myopress catheter is 30 cm long with an outer diameter of 1.05 mm. The
catheter has four sideholes with a total area of 1.5 mm2 at its terminal 1 cm.10 The
245
holes increase the contact area between the catheter and the tissue. The tip of the
catheter may be looked upon as a Guytons capsule53 extended to a cylinder. The
catheter has been proven to be suitable to record intramuscular pressure at rest with
injection,43 infusion,10,54 and noninfusion.10 The compliance of the pressure recording
system is 0.083 103 mL/mmHg if a transducer with a displacement of 0.57
106 mL/mmHg is used.10,47
Intracath Catheter
Matsen et al. used an Intracath catheter (Model 3166) to measure intramuscular
pressure at rest.22 The catheter was prepared by occluding the end hole with
adhesive cement and cutting four sideholes in the terminal 1 cm. The compliance
of the total pressure recording system is 0.25 103 mL/mmHg if pump infusion
is used.10
Wick-in-Needle
The device consists of a steel cannula with an outer diameter of 0.6 mm and a 3mm-long sidehole about 5 mm from the tip.44 Strands of nylon bers with a lament
thickness of 25 mm are pulled into the needle by a ne steel-wire loop. The compliance of the system is 0.06 mL/100 mmHg.
LOCATION
OF THE
TRANSDUCER
The transducer may be located outside the tissue such as in the traditional uidlled system or inside the tissue at the tip of the catheter. Transducer-tipped catheters
may be beroptic or solid-state intracompartmental catheters. Figure 16.8 shows
different transducer-tipped catheters.
Fiberoptic Transducer-Tipped Catheter
The pressure-sensing mechanism of the beroptic system (Model 420, Camino
Laboratories, San Diego, CA) is located at the tip of the catheter.39 The beroptic
catheter is inserted enclosed in a saline-lled sheath with an outer diameter of
2.1 mm and with 12 sideholes at the tip (Figure 16.8A). The contact area between
muscle tissue and the catheter tip is 9.6 mm2. The volume of the catheter and
the sheath in the muscle is 157 mm3. The compliance of the system is 5
106 mL/mmHg.
Solid-State Intracompartmental Catheter (STIC)
The STIC catheter is made of noncompliant polyethylene tubing. It has a 10-cmlong curved tip with 52 sideholes, which provide a total contact area of 8.3 mm2
with the tissue.45 A three-channel connector is attached to the catheter and then a
Millar Micro-tip transducer (No. PC-340, Millar Instruments, Inc., Houston, TX).
The catheter needs to be inserted by a 14-gauge needle. The cable of the Millar
transducer is 120 cm long and has an outside diameter of 1.33 mm.
246
FIGURE 16.8 Principles of transducer-tipped catheters. (A) The beroptic transducer-tipped

catheter. 1: sending ber, 2: receiving ber, 3: moving diaphragm, and 4: plastic sheath with
12 sideholes. (B) The Kodiag catheter. 1: stainless-steel housing, 2: unicristalline piezo
semiconductor with a chip, 3: wires to the connector. The Codman catheter is constructed in
a similar way. The transducer is protected in a groove. (C) Principle for transducer-tipped
catheters with possibilities for injection or infusion. They may be combined with (STIC
catheter) or without (Millar Micro-tip catheter) a protective sheath.
Codman Catheter
The Codman transducer-tipped catheter has been developed for measuring intracranial pressures (Figure 16.8C). It has been evaluated for intramuscular pressure
measurement.55 It may be classied as a noninfusion intracorporal pressure transducer. The transducer element consists of a silicon chip with pressure-sensitive
resistors forming a bridge. The integrated strain gauge is housed in a titanium case
(diameter 0.7 mm) which is placed at the tip of a Teon catheter. The membrane of
the pressure transducer is countersunk in the catheter to avoid artifacts due to
mechanical contacts with the surrounding tissue. This is important because solid
pressures in the tissue will not affect the transducer. The transducer is electrically
connected to a digital monitor. The working range is 50 to +250 mmHg. The
stability of the microsensor is good. The long-term drift is less than 0.8 mmHg per
24 h. The temperature drift is less than 0.03 mmHg/C.
The Kodiag Catheter
The Kodiag catheter consists of a piezoresistive pressure-recording system (Figure
16.8B). It consists of a reusable probe that is 60 cm long and has an outer diameter
of 0.99 or 1.32 mm (French size 3 or 4).56 The catheter is connected to a hand-held
battery-powered device. Like all unprotected transducer-tipped catheters, it should
247
TABLE 16.1
Classification of Common Pressure-Recording Principles (Infusion,
Noninfusion, and Injection) for Intramuscular Pressure
Measurements Related to the Medium of Signal Transmission
Saline
Electricity
Light
Ref.
Infusion
Pump infusion
Microcapillary infusion
STIC
Wick catheter
Slit catheter
Camino catheter (FOTT)
Codman catheter
Kodiag
+
+
+
23
10
39
Noninfusion
+
+
+
+
32
35
38
55
56
36
Injection
Needle injection
be inserted parallel to the muscle bers to avoid contact with muscle and tendon
that may press on the sensing area of the probe. If this is the case, the catheter reads
forces from the solid structures of the tissue. One advantage of transducer-tipped
catheters compared with uid-lled systems is their lack of hydrostatic artifacts
when subjects raise or lower their extremities. They are easy to use.
Disadvantages include the possibility of the sensor of the catheter tip to be
affected by solid components of the interstitial space. Therefore, the sensor must be
protected from contact with the solid structures by a protective covering sheath or
by a small measuring window. The intramuscular pressure recording may be performed as a noninfusion technique as in the beroptic transducer-tipped catheter39
and the Kodiag piezoresistive system.57 It may also be performed as an infusion
technique as in the STIC catheter method.45
MEDIUM
OF
SIGNAL TRANSMISSION
The medium through which the signal is transmitted may be saline, light, or electricity (Table 16.1). It is the sensor that converts the physical measurand to an
electrical signal. One example of this is uid-lled catheters in which the hydrostatic
saline pressure is converted by the transducer into an electrical signal.
TECHNIQUES FOR INTRAMUSCULAR

PRESSURE MEASUREMENTS
Direct methods for intramuscular pressure measurements include needle injection techniques,20,35,37,50 infusion techniques,22,58 and noninfusion techniques.33,34,36 Transducer-
248
TABLE 16.2
Ten Different Catheter Designs and Techniques for Measuring
Intramuscular Pressure at Rest in Humansa
Catheter Design
Needle
Wick-in-needle
Wick catheter
Myopress catheter
Slit catheter
Intracath catheter
Injection
Infusion
Fluid-Filled Systems
+
+
+
+
+
Noninfusion
+
+
+
Transducer-Tipped Systems
Fiberoptic transducer-tipped
STIC catheter
+
Kodiag
Codman
+
+
+
+
+
+
+
Fluid-lled systems are divided into injection, infusion, and noninfusion methods.
The transducer-tipped techniques are divided into infusion and noninfusion methods.
tipped techniques3840,59,60 may be used with or without infusion. The servo-null technique
that uses a micropipette16,61 is not discussed here. Different catheter tip designs may be
combined with different techniques for pressure measurements (Table 16.2).
INJECTION TECHNIQUES
Landerer rst described the needle injection technique in 1884. It consists of a uidlled needle or a pressure catheter, transducer, three-way stopcock, a syringe, and
a manometer (Figure 16.9). Since then the technique has been rened,35,62 evaluSyringe
Air
Meniscus
Saline
Needle
Air
Stopcock
FIGURE 16.9 Needle injection technique by a manometer.
Manometer
249
ated,20,36,43 and applied for clinical use.43,50,63 It can only be used to measure pressures
at rest. The needle injection technique has been shown to be less accurate for pressure
recordings at rest compared to other techniques.36,43,64 The injected volume through
an injection needle and the small contact area, over which equilibrium takes place,
increases the measured tissue pressure articially. In later studies,37,65 the recommended volume of 0.1 to 0.3 mL far exceeds the 0.1 to 0.5 mL that was used in
earlier studies.35 Also, the design of the needle tip has been changed since then.
With the needle injection technique, tissue pressure has been taken as the manometer
reading at the moment when the saline meniscus just moved66 or when it steadily
moved,37,67 or when the airsaline meniscus interface changed from concave to
straight.43 This means that pressures were taken during injection in the rst two
cases and immediately following injection in the third case.
The lack of sensitivity by the needle injection technique may be due to the low
uid conductance in a normally hydrated tissue and on the small cross sectional
area of the needle tip, which leads to a small contact area with the tissue.20,68 This
results in a high uid resistance. Therefore, pressure measurements during injection
give articially high intramuscular pressure reading,43 which is illustrated in Figure
16.10. Measurements of hydrostatic pressure in normally hydrated tissues are not
possible with injection techniques (Figure 16.10A). The rate of injection inuences
the measured pressure, which is illustrated in Figure 16.10C.
INFUSION TECHNIQUES
There are two types of infusion techniques: the constant pump infusion
technique22 and the microcapillary infusion technique.10 The difference between
Pressure
40 mmHg
10 sec.
20
0
40 mmHg
20
0
a.
b.
c.
10 sec.
Time
FIGURE 16.10 Results of intramuscular pressure recordings from a needle with sideholes
(upper trace) and without sideholes (lower trace). Magnitudes of pressure recordings during
injection depend on the time duration of the injection. Start of injection is indicated by arrow
up and end of injection by arrow down. Intramuscular pressure at rest after injection is
signicantly higher following injection by a needle without sideholes.
250
Pressure (mmHg)
15
10
Infusion rate
0
0
0.1
10
mL/h
FIGURE 16.11 Intramuscular pressure at rest depends on the infusion rate. It is fairly constant when infusion rates are kept between 0.1 and 3.0 mL/h. Most of the time intermittent
infusion rates of 0.1 to 0.3 mL/h are sufcient for recordings up to 24 h.
the two methods concerns only intramuscular pressure recordings during exercise.
Therefore, they will be discussed in more detail in Chapter 17. These techniques
may be combined with several catheter tip designs. The amount of uid infused
affects the level of intramuscular pressure recorded.10 However, in normally
hydrated anterior tibial muscle, pressure did not increase during 30 min with an
infusion rate of between 0.1 and 3 mL/h. Pressure was about 4 mmHg without
infusion and increased to about 6 mmHg when infusion was 0.1 mL/h. Figure
16.11 illustrates that there is a fairly wide range of low infusion rates that does
not signicantly affect intramuscular pressure at rest. It is well known that large
volumes of uid are required to cause even a slight additional increase of normal
interstitial uid pressure.68 Substantial amounts of uid can be added to the
interstitial space of skeletal muscle with only small alterations of the tissue uid
pressure.69 The relation between infused volume into muscle and intramuscular
pressure at rest has been documented for shoulder muscles,70 lumbar back muscles,54 and leg muscles.10,27
NONINFUSION TECHNIQUES
Fluid-lled catheter systems with external transducers, which are not injected
or infused, have been used extensively.33,36 Many catheter designs have been
251
combined with noninfusion techniques to measure intramuscular pressure.33,36,52,71 The noninfusion technique is required when measuring the uid
hydrostatic pressure of a normally hydrated tissue.34,44,51,72 Most noninfusion
techniques require a small amount of uid to be injected initially. However, no
injection or infusion is allowed during the recording. If this is the case, the
method is no longer a noninfusion technique.
INTRAMUSCULAR PRESSURE MEASUREMENTS

IN A SUBATMOSPHERIC ENVIRONMENT
Subatmospheric pressure has been applied on human limbs to study blood circulation, transcapillary uid dynamics,16,73 and countermeasures in simulated microgravity.74 The Myopress catheter combined with microcapillary infusion technique and
the beroptic transducer-tipped catheter (Model 110-D, Camino Laboratories, San
Diego, CA) is suitable to measure intramuscular pressures in the leg when the
pressure in the chamber varies between atmospheric and 100 mmHg.75
METHODS FOR NONINVASIVE MEASUREMENTS

OF INTRAMUSCULAR PRESSURE
An indirect method to estimate intramuscular pressure in the leg was described by
Kjellmer.76 Pressure measurements were based on the following considerations:
(1) ow through a collapsible tube can occur only when the pressure inside the tube
is at least as high as that outside; (2) venules and veins are collapsible tubes; (3)
tissue pressure acts directly on the venules and veins; and (4) intravascular pressure
in the venules and veins can never be lower than the tissue pressure.76,77 By recording
arterial pressure in the contralateral thigh, venous outow in the popliteal artery,
and leg volume, the maximal tissue pressure in the leg was obtained from distensibility curves of the veins.76
Pressure in the anterior compartment was estimated by auscultation over the
anterior tibial artery. Willey et al. estimated intramuscular pressure in the anterior
compartment by auscultating the Korotkoff sounds over the anterior tibial artery
above the ankle joint at rest and after exercise in the elevated limb.78 The height (H)
above the heart at which the sounds disappeared was measured. Compartment
pressure (P) was calculated as the brachial diastolic pressure (D) minus the hydrostatic pressure due to the height of the column (H) in centimeters:
P = D 0.8H
(16.3)
The coefcient 0.8 is calculated from the specic gravity of blood (1.06 g/cm3) and
mercury (13.6 g/cm3).
Steinberg and Gelberman measured quantitative hardness of leg muscles. They
used a low-friction probe connected to a plunger, a Teon seal, and a hard plastic
housing. Because the displacement of the plunger was directly proportional to the
pressure in the probe, they could calculate the displacement of the plunger for any
252
pressure. They found that hardness of the muscle correlated well with actual invasive
intramuscular pressure measurements.79
SUMMARY
No single method for intramuscular pressure measurement is superior to all methods.
The choice of method must be based on pressure to be measured, clinical setting,
and duration of intramuscular pressure recordings. The choice of method is inuenced by economical aspects, whether the pressure is recorded at rest or during
exercise, or both, with the subject lying supine, or whether the exercise includes
complex movements.
The most important requirements for the pressure-recording system are that it
must be stable, robust, and easy to calibrate. The size of the sensor must be small,
preferably 0.3 to 0.6 mm in diameter, to minimize physiological reactance. The
diameter of catheters for intramuscular pressure recordings should not exceed 1 mm.
Injection techniques are prone to erroneously high intramuscular pressure readings.
Electromanometry and intramuscular pressure measurements have a signicant
learning curve.
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5. Rorabeck, C.H. and MacNab, I., Anterior tibial compartment syndrome complicating
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12. Styf, J., Forsblad, P., and Lundborg, G., Chronic compartment syndrome in the rst
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30. Sadamoto, T., Bonde-Petersen, F., and Suzuki, Y., Skeletal muscle tension ow pressure and EMG during sustained isometric contractions in humans, Eur. J. Appl.
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31. Brace, R.A., Progress toward resolving the controversy of positive vs. negative interstitial uid pressure, Circ. Res., 49, 281, 1981.
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32. Fadnes, H.O. and Aukland, K., Protein concentration an colloid osmotic pressure of
interstitial uid collected by the wick technique: analysis and evaluation of the
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39. Crenshaw, A., Styf, J.R., Mubarak, S., and Hargens, A.R., A new beroptic transducertipped catheter for measuring intramuscular pressures, J. Orthop. Res., 8, 464, 1990.
40. McDermott, A.G.P., Marble, A.E., Eng, P., and Yabsley, R.H., Monitoring acute
compartment pressures with the STIC catheter, Clin. Orthop., 190, 192, 1984.
41. Aukland, K. and Wiig, H., Hemodynamics and interstitial uid pressure in the rat
tail, Am. J. Physiol., 247, H80, 1984.
42. MacEachern, A.G., Fox, R.H., and Gardner, A.M.N., The venous foot pump, J. Bone
Jt. Surg., 68-B, 667, 1986.
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44. Fadnes, H.O., Reed, R.K., and Aukland, K., Interstitial uid pressure in rats measured
with a modied wick technique, Microvasc. Res., 14, 27, 1977.
45. McDermott, A.G.P., Marble, A.E., Yabsley, R.H., and Phillips, B., Monitoring dynamic
anterior compartment pressures during exercise, Am. J. Sp. Med., 10, 83, 1982.
46. Burton, A.C. and Yamada, S., Relationship between blood pressure and ow in human
forearm, J. Appl. Physiol., 4, 329, 1951.
47. Styf, J., Chronic anterior compartment syndrome of the lower leg, Ph.D. Thesis,
University of Gteborg, 174 pp., 1986.
48. Landerer, A.S., Gewebspannung in ihrem Einuss auf die rtliche Blutbewegung
und Lymphbewegung, Vogel Leipzig, 1884.
Thesis, University of The Hague, 27, 1968.
51. Snashall, P.D., Lucas, J., Guz, A., and Floyer, M.A., Measurement of interstitial uid
pressure by means of a cotton wick in man and animals: an analysis of the origin of
the pressure, Clin. Sci., 41, 35, 1971.
52. Styf, J., Crenshaw, A., and Hargens, A., Comparison of non-infusion and non-constant
infusion techniques, Acta Orthop. Scand., 60, 593, 1989.
53. Guyton, A.C., A concept of negative interstitial pressure based on pressures in
implanted perforated capsules, Circ. Res., 2, 399, 1963.
55. Palmerud, G., Sporrong, H., Herberts, P., and Styf, J., Comparison of non-infusion
transducer-tipped catheter and a uid lled catheter with an extra-corporal transducer
for measuring intramuscular pressure, in preparation, 2003.
255
56. Willy, C., Gerngross, H., and Sterk, J., Measurement of intracompartmental pressure
with use of a new electronic transducer-tipped catheter system, J. Bone Jt. Surg., 81A, 158, 1999.
57. Evers, B., Becker, H.P., and Gerngross, H., Messung des Kompartmentdruckes mit
einem neuen piezoresistiven system, Hefte zu der Unfallchirurg, 267, 98, 1998.
58. McMaster, P.D., Intermittent take-up of uid from the cutaneous tissue, J. Exp. Med.,
73, 67, 1941.
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in the microcirculation of frogs mesentery, Am. J. Physiol., 207, 173, 1964.
62. Wells, H.S., Youmans, J.B., and Miller, D.G., Tissue pressure (intracutaneous subcutaneous and intramuscular) as related to venous pressure capillary ltration and other
factors, J. Clin. Invest., 17, 489, 1938.
75-A, 231, 1993.
65. Awbrey, B.J., Sienkiewicz, P.S., and Mankin, H.J., Chronic exercise induced compartment pressure elevation measured with a miniaturized uid pressure monitor: a
laboratory and clinical study, Am. J. Sp. Med., 16, 610, 1988.
66. Hargens, A.R. and Mubarak, S.J., Laboratory diagnosis of acute compartment syndromes, in Compartment Syndromes and Volkmanns Ischemic Contracture, Mubarak,
S.J. and Hargens, A.R., Eds., W.B. Saunders, Philadelphia, 1981, p. 110.
68. Guyton, A.C., Interstitial uid pressure: pressure volume curves of interstitial space,
Circ. Res., 16, 452, 1965.
Physiol. Scand., 90, 583, 1974.
71. Shakespeare, D.T., Henderson, N.J., and Clough, G., The slit catheter: a comparison
with the wick catheter in the measurement of compartment pressure, Injury, 13, 404,
1982.
72. Guyton, A.C., Granger, H.J., and Taylor, A.E., Interstitial uid pressure, Physiol. Rev.,
51, 527, 1971.
73. Lnne, T., Edfeldt, H., Quittenbaum, S., and Lundvall, J., Large capillary uid
permeability in skeletal muscle and skin of man as a basis for rapid benecial uid
transfer between tissue and blood, Acta Physiol. Scand., 146, 313, 1992.
74. Hargens, A.R., Recent bed rest results and countermeasure development at NASA,
Acta Physiol. Scand., 150 (Suppl. 616), 103, 1994.
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256
77. Permutt, S. and Riley, R.L., Hemodynamics of collapsible vessels with tone: the
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78. Willey, R.F., Corall, R.J.M., and French, E.B., Non-invasive method for the measurement of anterior tibial compartment pressure, The Lancet, 13, 595, 1982.
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17
Measurements of
Intramuscular Pressure
during Exercise
INTRODUCTION
History and clinical signs alone are often insufcient to establish the diagnosis of
chronic compartment syndrome.13 However, they are valuable tools in selecting
patients with chronic exercise-induced pain for intramuscular pressure measurements.3,4 Therefore, measurement of intramuscular pressure during or at rest after
exercise has an important role in diagnosis of the syndrome.
Measurements of intramuscular pressure during exercise are also useful in physiological research and in the study of muscle biomechanics.1,512 They are also
valuable to study limb function,1318 limb swelling during and at rest after exercise,3,10
and force generation during muscle contraction.5,7,1922
Different techniques for direct pressure measurements used in clinical situations
are discussed in this chapter. Most of the methods have been thoroughly evaluated
and are generally accepted for pressure measurements at rest but not for measurements during exercise. Every technique for intramuscular pressure measurement has
its own advantages and disadvantages. Before a technique for intramuscular pressure
recording is selected, it is important to determine the exercise protocol. Will the
pressure be measured at rest or during exercise, or both? Will the patient exercise
on an ergometer in the laboratory or run outdoors? What is the size of the compartment? The answers to these questions are helpful in selecting an optimal and suitable
pressure-recording technique. The dynamic properties of a pressure-recording system are most important for accurate measurements of intramuscular pressures during
exercise. Therefore, a substantial part of this chapter is focused on this issue.
DYNAMIC PROPERTIES OF PRESSURE-RECORDING

SYSTEMS
Signals may be classied as static or dynamic. Static and dynamic properties of a
pressure-recording system must fulll certain criteria to allow for proper recordings
of intramuscular pressures during exercise. All static nonlinearities discussed in Chapter XVI can also affect dynamic responses. Accuracy of an intramuscular pressure
recording can be expressed as the difference between the true value and the measured
value divided by the true value. The ratio is expressed in percent. The dynamic
accuracy of a recording system is the delity with which the system reproduces a
257
258
Pressure
Time
FIGURE 17.1 The dotted line indicates the true applied pressure (arrow up). The continuous
line indicates the recorded pressure. The pressure rises slowly to the new value in overdamped
recording systems. It decreases slowly to the initial value when pressure is released (arrow down).
dynamic event. Errors of the dynamic accuracy can have serious diagnostic consequences when intramuscular pressures are recorded during exercise in clinical practice
and in research. For instance, if the pressure-recording system is overdamped, which
means that the bandwidth is too low, physiological pressure changes during muscle
contraction and muscle relaxation (that is, or pressure in the relaxed muscle between
contractions) cannot be measured.3,9 Therefore, chronic compartment syndromes cannot be diagnosed by pressure recording during exercise with such a technique.9
However, they may be diagnosed by pressure recording at rest after exercise.
In overdamped pressure-recording systems, the recorded intramuscular pressure during a constant muscle contraction will rise slowly to the new value without
oscillations (Figure 17.1). Overdamped systems are therefore unsuitable for
recordings of fast dynamic events. They are also subject to time delay. One example
of this is intramuscular pressure recording by the wick catheter system during
dynamic muscular activity (Figure 17.2). As will be discussed next, they are also
unsuitable for measurements of mean intramuscular pressures during repeated
muscular contractions.
In underdamped recording systems, the pressure during a muscle contraction
rises rapidly to the new value. It oscillates at its new damped natural frequency
(Figure 17.3). The pressure oscillations fade away at a rate determined by the degree
of damping in the system.
Several of the methods used for intramuscular pressure measurements at rest
have been applied to measure pressures during exercise in clinical diagnosis13,16,23,24
and to estimate muscle load in physiologic studies.5,7,1922 However, the dynamic
properties of the pressure-recording system have been evaluated in only a few
reports.9,20,25 The dynamic properties must be known to permit proper interpretation
of intramuscular pressure recordings during exercise. The dynamic properties of a
uid-lled catheter manometer system depend on catheter materials, lengths, inner
diameters, number of connectors, and the compliance of the whole catheter manometer system. The interaction on the measuring system of the various parameters is
rather complex. Therefore, all dynamic measurements of intramuscular pressure
should be preceded by dynamic calibration of the method. The dynamic properties
Measurements of Intramuscular Pressure during Exercise
259
Time
Seconds
200 mmHg
MCI
200 mmHg
Wick
FIGURE 17.2 Intramuscular pressure recordings with a microcapillary infusion technique

(MCI) (upper trace) and an overdamped noninfusion system with the wick catheter (lower
trace) from the same spot in the tibialis anterior muscle of one patient. Recording by the wick
catheter system does not allow for measurement of intramuscular pressure during muscle
contraction or during muscle relaxation with a contraction frequency of 1 Hz. The rise time
for the wick catheter may be up to several seconds.
of a pressure-recording system can be determined by measurements of rise time (or

response time), the compliance, and the natural frequency (or resonance frequency)
of the pressure-recording system.
RISE TIME
The rise time (Tr) is used to estimate the dynamic properties of a pressure-recording
system. The rise time can be calculated by the pressure step-function technique. The
Pressure
Time
FIGURE 17.3 In underdamped recording systems, the signal will rapidly rise to the new
value and oscillate around it. When pressure is released (arrow down), it will oscillate around
the new value.
260
Pressure
100%
90%
10%
0
Tr
Time
Td
FIGURE 17.4 The rise time can be calculated by the pressure step-function technique. Rise
time (Tr) for a pressure-recording system is dened as the time period required for the output
signal to pass through the range of 10 to 90% of its nal value. Time delay (Td) is the time
period required for the signal to reach its nal value.
rise time for a pressure-recording system is dened as the time period required for
the output signal to pass through the range of 10 to 90% of its nal value as a
response to a step-like input signal (Figure 17.4).
If the overshoot of the response is less than a few percent and if the rise time
(Tr) for a system is known, the frequency bandwidth (B) may be calculated by the
following equation:
TR B = k
(17.1)
where the constant k is 0.35. The wick catheter system is an overdamped system
because the stranded wicks prevent rapid uid ow over the tip of the catheter. It has
a rise time of up to 4 sec.9 By substituting this number into Equation 17.1, the frequency
bandwidth will be about 0.1 Hz. This means that the duration of a contraction must
be at least 5 sec followed by a relaxation of 5 sec to allow for an accurate measure of
the contraction and relaxation pressures during exercise. This also implies that the
maximum contraction frequency must not exceed 6 contractions/min (or 0.1 Hz).
The frequency bandwidth (B) is dened as the difference between the upper
frequency (fu) limit and the lower frequency (fl) limit.
B = fu fl
(17.2)
This means that the amplitude of the pressure curve is distorted and the readings
are not accurate if the contraction frequency is higher than the upper frequency limit
261
or lower than the lower limit. Most authors recommend a bandwidth that is at least
10 times higher than the signal to be recorded. The frequency bandwidth of a recorder
should always be greater than that of the signal.
COMPLIANCE
OF
PRESSURE-RECORDING SYSTEMS
The compliance (C) of a transducer is the relation between the volume change (DV)
and the pressure change (DP), given by Equation 17.3:
C = DV/DP
(17.3)
The compliance of the diaphragm is much higher than that of the saline-lled catheter
or transducer cavity, provided the saline solution is bubble-free and the catheter
material is relatively noncompliant.
A crucial part of the preparation for pressure recordings is lling the transducer
and the transducer line with saline that is free of entrapped air bubbles and then
keeping it free of air bubble formation. Even ne bubbles in the recording system
increases the total compliance considerably and may decrease the bandwidth by
decreasing the high frequency limit. Again, because air bubbles may be invisible, it
is important to have some means for testing the dynamic performance after lling.
If cold saline from the refrigerator is used, air bubble formation will increase in
room temperature. The same is true when saline of room temperature in the catheter
is exposed to the warm (35 to 38C) skin and muscle tissue during exercise. Minimizing compliance is the greatest problem in obtaining good dynamic properties of
the intramuscular pressure-recording system. One should look for air bubbles and
leaky connections if the bandwidth of the recording system is low or the compliance
is high. The compliance of the total intramuscular pressure-recording system, i.e.,
the catheter and transducer, should be less than 0.25 mm3/100 mmHg.9,26,27
NATURAL FREQUENCY
The natural frequency (Fn) is the frequency at which the pressure-recording system
would resonate in the absence of any damping. The natural frequency (or resonant
frequency) is inuenced by length, radius, and compliance of the pressure-recording
system. When a pressure applied to a pressure-recording catheter is suddenly
changed from one level to another, the system will resonate at the damped resonant
frequency. The natural frequency (Fn) of the system is given approximately by:
Fn = 1 2 p A 2 M C
(17.4)
where A is the piston area of the transducer, M the uid mass of the pressurerecording system, and C the compliance of the system. By Equation 17.4 it is possible
to explain why a constant pump infusion technique has slower dynamic properties
than those of the microcapillary system. The pump infusion technique has a significantly larger volume of saline that is uid mass in the pressure-recording system.9
262
The dampening ratio is the natural logarithm of the amplitudes of the rst and
second oscillations in the response to the step function.28,30 The duration of the
oscillations depends on the damping. Optimal damping factor is about 0.7. The
duration of the oscillations depends on the damping. The higher the bandwidth (or
the natural frequency) of the system, the wider the range of frequencies over which
the correct amplitude will be recorded. Also, movement artifacts of a catheter are
amplied in a high-frequency response system.
In a recording system, pressure is transmitted nearly at the velocity of sound in
water, which is about 1400 m/sec. Therefore, the time period it takes for a pressure
wave to travel down the catheter and transducer line is less in relation to the period
of the resonant frequency.
DYNAMIC TESTING OF PRESSURE-RECORDING

SYSTEMS
A transducer is a device that converts energy from one form to another. As described
in Chapter 16, transducers must be tested for stability, sensitivity, linearity, hysteresis,
and volume displacement. The resonance frequency of the pressure-recording system
may be used to judge dynamic properties of the system. This is most important
because many factors, including different catheter materials and catheter dimensions
and the experimental setup, may affect frequency response.3,9,29 The ideal pressurerecording system should have a linear response, which is independent of frequency
over the range of interest. Dynamic calibration of manometer systems can be tested
in at least two ways, with techniques that generate pressure step response and
sinusoidal pressure waveforms.28,31
TRANSIENT STEP RESPONSE

The basis for this method is to apply a sudden step input to the pressure catheter
and to record the output of the system (Figure 17.3). It is simple and most easy to
perform. Performance of the pressure-recording system may be expressed as rise
time in milliseconds as illustrated in Figure 17.4.
SINUSOIDAL PRESSURE GENERATOR

Frequency response of the system is a more accurate method but is more complicated
to perform and requires a sinusoidal pressure generator. The equipment to generate
a sinusoidal pressure wave is complex.31 Measurements with underdamped systems
may give a hump in a frequency responseamplitude curve, as illustrated in Figure
17.5. The hump contains the resonant frequency.
It is important to have a high resonant frequency, at least 10 times or more than
the highest frequency considered to be important in the original waveform. Generally
a frequency response exceeding the event to be measured by up to 20 Hz is required
to record the amplitude of the event accurately.32 A frequency response greater than
40 Hz is required to limit errors to 10%.32
263
Amplitude
fl
fu
Frequency
FIGURE 17.5 Measurement by an underdamped system gives a hump (arrow), which contains the resonant frequency in the frequencyamplitude curve; fu is the upper frequency limit
and fl is the lower frequency limit.
Underdamped systems may be treated by partial clamping of the transducer line

close to the transducer. The amplitude response should be at without resonant
peaks. This will optimize the system as regards a fast rise time and minimize
distortion of the amplitude.
PRACTICAL RECOMMENDATIONS
PRESSURE-RECORDING SYSTEMS
The following steps are helpful in maintaining high dynamic properties of the
pressure-recording system: (1) Using high-quality stopcocks and a minimum number
of Luer locks. (2) Applying a known pressure and closing the stopcocks. If the
pressure falls within a few minutes, then there is a signicant leakage. (3) Testing
transducers, ampliers, and recorders for noise, linearity, stability, and hysteresis.
(4) Conducting the transient dynamic test regularly at the end of the procedure. Most
publications on measurements of dynamic intramuscular pressure recordings lack
documentation of transient testing. (5) Applying damping of an underdamped catheter manometer system by constricting the transducer line close to the transducer
with a binding screw.
CATHETER INSERTION TECHNIQUE

Catheters for intramuscular pressure recordings during exercise must be inserted
as atraumatically as possible. The introducer and the catheter should be inserted
as parallel to the muscle bers as possible and with the cutting tip of the needle
retracted within the plastic sheath of the introducer (Figure 17.6). Once the introducer has penetrated the skin and the fascia, the tip of the needle should be
withdrawn into the plastic sheath of the introducer. In this way, damage to the
muscle ber is minimized. Surrounding muscle bers help guide the plastic sheath
264
Incorrect
Correct
catheter
skin
fascia
muscle
tendon
FIGURE 17.6 Catheters for intramuscular pressure recordings during exercise must be
inserted parallel with the muscle bers to allow for a pain-free investigation and minimize
the risks for catheter bending. The catheter tip must not be inserted too close to the central
tendon. The distance (d) between the tip of the catheter and muscle tendon must allow for at
least a 20% muscle ber shortening during contraction.
at insertion into the direction of least resistance, which is parallel to the bers.
Once the catheter is in place, this allows the muscle bers to slide over the catheter
tip in a parallel fashion during concentric and eccentric muscular activity. In this
way, physiologic reactance to the measurement is minimized. That means that the
patient or subject experiences less discomfort during muscular activity and will
be able to exercise his/her muscles in a normal way without pain inhibition.
Knowledge of the pennation angle and muscle ber length is a prerequisite for a
successful catheter insertion and a reliable measurement of intramuscular pressure
during exercise.
Intramuscular pressure is a function of the depth of the catheter in the muscle.
Depth is dened as the number of layers of muscle bers that cover the catheter
tip. In many cases, depth of the catheter is dened as the distance from the
centrally located tendon within the muscle to the tip of the catheter, and not the
distance from the skin or fascia.33 Catheters should be placed in a standardized
way to a depth that will allow the muscle bers to shorten 20% of their resting
length during contraction without the tendon hitting the catheter tip. If the tendon
hits the catheter tip during concentric contractions, two problems may occur:
(1) The patient may experience the muscle contraction as painful. In such cases,
the patient cannot perform maximal contractions due to pain inhibition. Also,
intramuscular pressure between contractions may be elevated because of the
patients inability to relax his/her muscles. (2) The tip of the catheter may become
bent, which may create partial occlusion, which will decrease dynamic properties
of the pressure-recording system. In rare cases the catheter may become completely occluded.3,34
CHECK
OF
265
CATHETER POSITION
Catheter position can be checked by sonography35 or a function test.36 By asking

the subject to rotate different joints, different muscles in the compartment will be
activated. Catheter location can be conrmed by the pressure response to these
movements (Figure 17.5). External compression by a constant force by the investigators ngertip in a proximodistal direction over the catheter tip may identify
location of the catheter. The location of catheter tip can be determined by measuring
the maximal pressure amplitude response to external compression by the investigators ngertip (Figure 17.4).
POSITION
OF THE
LIMB
Position of the subject, position of the joint over which the muscle acts,35,37 and
external compression from the underlying surface must be controlled because they
affect intramuscular pressure. The heart level, which is dened as being 5 cm below
the manubrium sterni in a supine subject, is a common reference point. One must
be aware of the hydrostatic effects in sitting and standing patients as well as when
they perform complex movements of a limb.
TYPICAL DISTORTIONS OF INTRAMUSCULAR

PRESSURE RECORDINGS
In an underdamped system, the amplitudes of the higher-frequency components of
the pressure wave are amplied. In such a system, it may be difcult to measure
the exact pressure level during dynamic exercise. For an overdamped system, these
higher-frequency components are attenuated. Overdamped systems such as the noninfusion system with a wick catheter show a time delay of up to several seconds
(Figure 17.7).9 The risk for partial occlusion of pressure catheter increases when
noninfusion systems are used (Figure 17.8).34 The transducer-tipped Camino catheter
measures negative pressure values between concentric muscular contractions that
are during muscle relaxation pressure.25 This may be explained by the piston effect
due to the fairly large size of the catheter. The large size of the catheter may create
a negative interstitial uid pressure as the muscle bers slide over the tip of the
Camino catheter (Figure 17.9).
Another explanation may be that the tip of the catheter was directed toward
interstitial uid ow direction during contraction and from the uid ow direction
during muscle relaxation. The uid hydrostatic pressure sensed by a transducer varies
with the direction of the uid ow. The variation is due to the kinetic energy of the
uid. The total uid pressure (Ptotal) per unit volume is dened by Bernoullis
equation:
Ptotal = P0 + dgh + dv2/2
(17.5)
where P0 is the static pressure with no ow, d the density (g/cm3), g the acceleration
due to gravity (g = 9.81 m/sec2), h the height above the reference level, and v the
266
5 sec
100
40
100 mmHg
40
100 mmHg
Wick
100
MCI
A
FIGURE 17.7 Intramuscular pressure recordings by the wick catheter (no infusion) (upper
trace) and the microcapillary infusion techniques (infusion rate is 1 mL/h) (lower trace).
Catheters are located next to each other in the same muscle. (A) Pressure recording during
concentric muscular activity. Equilibrated pressures during muscle contraction and muscle
relaxation cannot be obtained by the wick method due to the slow response. Recording by
the wick catheter method is a frequency-dependent artifact. (B) It takes a longer time for the
wick method to reach the equilibrated intramuscular pressure at rest after exercise. (C) Both
catheters are ushed by 0.1 mL of saline. Pressure at rest in the ushed wick catheter is
signicantly increased. (D) The dynamic properties of the wick catheter system improve
following injection, but not to the level of the infusion method. In this case, muscle contraction
pressures are obtained because of the long duration of the muscle contraction time. However,
the relaxation time is too short to allow for a proper recording of muscle pressures between
contractions, i.e., muscle relaxation pressure. (E) Intramuscular pressures at rest after exercise.
sec.
1 sec
200 mmHg
200 mmHg
Sin
200 mmHg
0
occl.
dx
A.
B.
FIGURE 17.8 (A) Arrow up indicates start of contractions and arrow down indicates end of
contractions. The pressure curve illustrates occlusion of the catheter tip. (B) Air bubbles in
the pressure-recording system may lead to incorrect measurements of intramuscular pressure.
The dynamic properties become impaired. The muscle contraction pressure in the upper trace
is too low (arrow).
267
Pressure (mmHg)
40
0
Time
FIGURE 17.9 Intramuscular pressure recording by a beroptic catheter with a large diameter
of the catheter tip. Pressure during muscle relaxation is negative initially due to a piston effect
at the tip of the catheter. After a few minutes of muscular activity the effect disappears,
possibly by normal edema formation around the tip of the catheter. The bars indicate the time
period for muscle relaxation.
uid velocity (m/sec). The Bernoulli equation may help to explain the difference
observed between transducer-tipped catheters with the transducer at the distal end
and the transducer at the side end of the tip. The area of the catheter tip in relation
to the total uid volume available around the tip may contribute to the piston effect
and make the contribution of uid energy by uid ow more pronounced by large
catheters without sideholes.
TECHNIQUES FOR INTRAMUSCULAR PRESSURE

MEASUREMENTS
Different techniques for direct pressure recordings may be classied as injection
techniques, infusion techniques, noninfusion techniques, transducer-tipped techniques. Most of the methods have been thoroughly evaluated and are generally
accepted for intramuscular pressure recordings at rest.
The needle injection technique can be used to measure pressure at rest only.3841
This technique has been shown to be less accurate than the other techniques for
pressure recordings,40,4244 especially if pressure recordings are made during injection.44 The injection technique measures the tissues resistance to uid ow and
gives an articially high reading if pressure is measured during injection. However,
a needle or catheter with one or multiple sideholes at its tip reduces the risk of
recording articially high pressures, especially when pressures are recorded by the
meniscus method following an injection.44
INFUSION TECHNIQUES
The constant pump infusion technique27 and the nonconstant microcapillary infusion
technique9 are both suitable for recording of intramuscular pressures at rest and
during exercise.9,16,45,46 The Intracath and Myopress catheters are uid-lled sys-
268
Pressurizer
Microcapillary
A.
Pressure tubings
Recorder
Stopcocks Transducers
B.
Syringe
FIGURE 17.10 The microcapillary infusion (A) and the pump infusion (B) methods. The
main difference between methods is the volume of the pressure-recording system, which is
much larger with the pump infusion method.
tems with extracorporal transducers. They are both specially designed with multiple
sideholes at their tip, which make them suitable to be used with infusion (Figure
17.10). However, they may be used without infusion as well. Both infusion techniques can be combined with different types of catheters, e.g., the Intracath, Myopress, Slit and STIC catheters.9,27,46 The saline volume of the pressure-recording
system is signicantly less in the microcapillary infusion system compared with that
in the pump infusion system. This helps improve the dynamic properties of the
microcapillary infusion system because a smaller volume of saline, i.e., a smaller
weight, has to be displaced in the measuring system.
The resonance frequency of the microcapillary infusion system is 27.8 Hz
compared to 7.7 Hz with the pump infusion system, as determined by the pressure
step-function technique.9 Applying the sinusoidal pressure generator resulted in
resonance frequencies of 31 and 9 Hz, respectively. During a 3-h period of pressure
recording, the resonance frequency fell from 31 to 17 Hz with the microcapillary
infusion technique, and from 9 to 6 Hz with the pump infusion technique, due to
formation of small air bubbles in the transducer line.9
The magnitude of the infusion rate is important. The compliance of muscle
tissue decreases during muscle contraction. Therefore, the risk of reading artifactually high muscle contraction pressure with the microcapillary infusion technique is
less than with the constant pump infusion technique. The reason for this is that the
infusion rate with the microcapillary infusion technique is minimal or even zero
during muscle contraction (Figure 17.11). The compliance of muscle tissue at rest
is high.47,48 Intramuscular pressure is fairly constant when 0.1 to 3.0 mL/h of saline
269
Infusion rate
1.5 ml/h
0
0
Intramuscular pressure
(150 mmHg)
FIGURE 17.11 The relationship between intramuscular pressure and infusion rate with the
microcapillary infusion technique. When intramuscular pressure approaches 150 mmHg, the
infusion rate is close to zero. It is 1.5 mL/h when intramuscular pressure is atmospheric.
is infused.9,11 However, infusion rates exceeding 0.2 mL/h are often unnecessary for
pressure recordings during intermittent exercise if a Teon catheter with an open tip
and multiple sideholes at its tip is used. The microcapillary infusion technique has
been combined with a Slit catheter,34 wick catheter,9 STIC catheter,8 Intracath,27
and a Myopress catheter.911,22
NONINFUSION TECHNIQUES
Different non-infusion techniques40,43 have been used to record pressures at rest and
during exercise.2,13,49,50 However, it has been shown that the wick catheter method
is unsuitable for recordings of intramuscular pressure during exercise because of its
poor dynamic properties.9,20 Pressure values during muscle contraction and muscle
relaxation depend on the contraction frequency as illustrated in Figure 17.12, as well
as on the relative time duration of muscle contraction and muscle relaxation. Pressures during exercise were not accurately recorded with a slit catheter because the
tip of the catheter occluded.34 For this reason, slit catheters must be ushed repeatedly
when pressures are recorded with a noninfusion technique.1,20,34,45 In this situation,
the device is no longer to be considered a noninfusion technique but rather an
intermittent injection technique. Figure 7.7 illustrates the improved dynamic properties of noninfusion systems following ushing of catheters. Furthermore, the tip
design of the slit catheter has been suggested to be more traumatic to the local tissue
during muscular activity.34 It has been described how the slits at the tip of the catheter
become deformed following intramuscular pressure measurements during exercise.
The tip design of Myopress and Intracath catheters make them suitable to be used
with noninfusion as well.
TRANSDUCER-TIPPED CATHETERS
Pressure-recording systems that are uid lled require ushing or infusion to maintain accuracy.9,27,34,43,46 These methods are equipped with external transducers and
270
10 sec
300 mmHg
300 mmHg
A.
B.
C.
FIGURE 17.12 Muscle contraction pressure and muscle relaxation pressure, i.e., pressure
between contractions in a relaxed muscle, during constant muscle load at (A) 75, (B) 37 and
(C) 18 contractions/min. The readings in the upper trace obtained with a microcapillary
infusion technique show the same magnitude of pressure values, independent of the contraction frequency. In the lower trace, the readings depend on the contraction frequency, because
of the prolonged rise time of the noninfusion system (Redrawn from Styf, J.R. and Krner,
L.M., Clin. Orthop. Rel. Res., 207, 253, 1986.)
are thus prone to hydrostatic artifacts when the limb position changes relative to the
level of transducer.
Transducer-tipped catheters may be classied as beroptic or solid state. These
catheters measure the pressure at the point at which it occurs. All the problems and
pitfalls that are associated with transmission of pressure through the transducer line
to an external transducer are eliminated. Transducer-tipped catheters are suitable for
recordings of muscle contraction pressure during complex movements of the extremity because they eliminate any problem of the changing hydrostatic column during
such movements. The catheters are also suitable for recordings of pressures at rest
after exercise. However, if the catheter has a large diameter, it is not recommended
for recordings of muscle relaxation pressure during exercise, because of the piston
effect.25 This effect gives negative pressure values during muscle relaxation, possibly
by the vacuum from sliding bers over the tip of the catheter. Catheters with a large
diameter are more prone to this effect. However, the effect diminishes after 5 to
10 min of exercise. The reasons for negative pressure recordings have been discussed
previously in this chapter.
Fiberoptic Catheters
The beroptic transducer-tipped system for intramuscular pressure measurement was
modied by Crenshaw et al. for measuring intramuscular pressure at rest51 and during
exercise.25 They showed that the beroptic system (Model 420, Camino Laboratories,
San Diego, CA) is most suitable to measure pressure during muscle contraction
especially when complex limb movements involve changes relative to the horizontal
271
plane. The beroptic catheter is enclosed in a sheath with an outer diameter of

2.1 mm lled with saline and with 12 sideholes at the tip. The contact area between
muscle tissue and the catheter tip is 9.6 mm2 and the compliance of the system is
5 106 mL/mmHg. The volume of the catheter is 157 mm3.
Optical transducers measure displacement of the diaphragm by optical means. The
main advantage of the new beroptic catheter-tipped pressure transducer is the small
size and the absence of electricity within the catheter, which makes it safer than other
systems. The magnitude of temperature drift of beroptic catheters is small.52
Other beroptic pressure sensors are based on silicon micromechanics. The
sensor body, which can be an interferometer of silicon, is placed on the end of an
optical ber. The sensor measures the modulation of light intensity, which occurs
by interference in the cavity when its depth is of the same order as the wavelength
of the light in the ber. The technique is based on the mechanical properties of
silicon. It has a volume displacement of 0.5 103 mm3/100 mBar. The diameters
of these catheters can reach 0.3 to 0.5 mm, which is a suitable size for biomedical use.
STIC Catheter
The solid-state intracompartmental (STIC) catheter is designed with an internal
silicon semiconductor strain gauge transducer.46 A multiperforated noncompliant
polyethylene tubing (PE260) is tightly tted over the tip of the transducer diaphragm.
The cross sectional area for uid ow through the perforations is 1.4 mm2. A curved
plastic sleeve with a troachar is used to insert the catheter in the muscle. The plastic
sleeve is 10 cm long and the inner diameter is 2.3 mm. The STIC catheter combines
the advantages of being transducer-tipped and has the possibility being infused. The
infusion can be both a constant pump infusion and a microcapillary nonconstant
infusion technique.
Solid-state transducers are based on silicon chips. In contrast to beroptic catheters, they do not require a specialized amplier. They can be connected to the
patient monitor via an inexpensive interface unit. Generally, they have fairly low
zero-drift good frequency response and stable linearity. One drawback is that they
cannot be rezeroed after implantation. A normal drift of 5 mmHg during 8 h is
considered to be normal for both uid-lled and transducer-tipped systems.
Codman and Kodiag Catheters
The Codman microsensor transducer (Codman, Johnson & Johnson, Raynham, MA)
was developed clinically for intracranial measurements. It has been modied and
tested for intramuscular pressure recordings.53 The catheter is small and exible and
made of nylon tubing, which makes it suitable for intramuscular pressure measurements during exercise. The dynamic properties of the system are high.
The transducer element is based on a silicon chip with diffused pressure-sensitive
resistors forming a bridge. It consists of an integrated strain gauge hosted in a
titanium case and placed close to the tip of a Teon catheter with a diameter of
0.7 mm. The membrane of the pressure transducer is countersunk in the catheter to
avoid artifacts due to mechanical contacts with the surrounding tissue. The pressure
transducer is electrically connected to a digital intracranial pressure monitor with
272
ne wires passing through the catheter. The working range is 50 to 250 mmHg.
The stability of the microsensor is good. The long-term drift is less than
0.8 mmHg/24 h and the temperature drift is less than 0.03 mmHg/C. The frequency response is excellent. The Codman catheter is also suitable for pressure
measurements during exercise. It withstands mechanical stress exerted on the tip
of the catheter during muscle contractions. Artifacts superimposed on the true
intramuscular pressure signal due to locomotion or vibration of the extracorporal
part of the catheter are eliminated. Another advantage of the Codman catheter is
that it has a smaller diameter than the beroptic transducer-tipped catheter. Patients
do not report as much discomfort during intramuscular pressure recordings during
exercise by this catheter.
The Kodiag catheter, described in detail in Chapter 16, may also be used for
intramuscular pressure recordings during exercise.
REFERENCE VALUES FOR INTRAMUSCULAR

PRESSURES
The following values of normal and abnormal intramuscular pressures in humans
refer to the supine position and with the tip of the catheter at the heart level.
AT
REST
BEFORE
EXERCISE
Normal Values
Normal pressures in most muscles vary between 2 and 8 mmHg3,9,16,40,45,5457 but
pressures up to 10 to 15 mmHg have been reported.2,8,58 The recorded pressure depends
on the method used, the position of the leg,35 and the depth of the catheter in the
muscle.33,59 Intramuscular pressures at rest are higher when injection or infusion
techniques9,43 are used or when the volume of the pressure-recording catheter is large.8
Abnormal Values
Intramuscular pressure at rest before exercise is high in patients with chronic compartment syndrome.2,3,9,16,57,58,60 However, the wide range of pressures at rest and
their dependence on the position of the ankle joint and the depth of the catheter in
the muscle, as well as the position of the subject, make the use of only this parameter
unreliable in the diagnosis of chronic compartment syndrome.33,35,59 Also, pressure
at rest before exercise may increase by active muscle tension from pain and by
external compression by the underlying surface. For these reasons, the use of this
pressure parameter alone is not recommended.3,4,29
MUSCLE CONTRACTION PRESSURE
DURING
EXERCISE
Muscle contraction pressure during exercise is an indicator of force generation of that

muscle.5,7,1922 Recording of muscle contraction pressure requires good dynamic properties of the pressure-recording system.8,9,11,22,25,61 The upper traces of Figure 17.2 and
lower trace of Figure 17.7 illustrate measurement of muscle contraction pressure during
273
Pressure
A.
B.
Time
FIGURE 17.13 (A) Normal pressure recording during exercise. (B) Muscle contraction pressure decreases at the end of exercise due to muscle fatigue. Muscle relaxation pressure remains
elevated due to the increased volume of the muscle.
exercise. Pressures during muscle contraction ranging from 100 to 250 mmHg have
been recorded in the anterior tibial and other muscles.3,5,6,8,9,12,19,20,22,25 This pressure
parameter is not directly related to the pathophysiology of chronic compartment syndrome and should not be used to diagnose the syndrome. Muscle contraction pressure
is often low at the end of exercise because the force generation decreases due to muscle
fatigue or pain-induced muscle weakness (Figure 17.13).
MUSCLE RELAXATION PRESSURE
DURING
EXERCISE
Normal Values
The magnitude of muscle relaxation pressure during exercise, i.e., the pressure
between contractions, depends on the volume load of the muscle. Muscle relaxation
pressure increases for two reasons. Postexercise edema increases the volume of the
muscle and the regional muscle blood ow increases, both of which increase intramuscular pressure. Therefore, intramuscular pressure normally increases from about
5 mmHg before exercise in the supine subject to 10 to 25 mmHg after
exercise3,9,10,12,62,63 depending on the muscle studied. In an upright subject, the muscle
relaxation pressure during exercise is lower than the pressure at rest after exercise.17
The reason for this is the effect of the calf muscle pump, which decreases blood
volume in the leg following muscular contractions. At rest after exercise, the intravenous hydrostatic column elevates the interstitial hydrostatic pressure in the leg.
Recording of muscle relaxation pressure requires good dynamic properties of the
pressure-recording system.8,9,11,22,25,61
Abnormal Values
Muscle relaxation pressures exceeding 35 to 55 mmHg correlate well with the
development of pain, swelling, and impaired muscle function in patients with chronic
274
seconds
200 mm Hg
40 mm Hg
left
200 mm Hg
40 mm Hg
right
FIGURE 17.14 Results of intramuscular pressure recordings from one patient with (upper
trace) chronic compartment syndrome and one without (lower trace) the syndrome. Muscle
contraction pressure and muscle relaxation pressure can be read at (A). By changing the
standard for intramuscular pressure from 200 to 40 mmHg, muscle relaxation pressure can
be read with higher accuracy (B). At rest after exercise, intramuscular pressure and the
amplitude of pressure oscillations are signicantly greater in compartment syndrome (D).
The elevated pressure is not normalized at 6 min (E) or at 10 min (F) after exercise.
compartment syndromes,3,4,29 to decreased muscle blood ow10 and decreased tissue

oxygenation in these patients.64 This pressure is related to the pathophysiology of
the syndrome and is the best pressure parameter to study during exercise in patients
with the chronic compartment syndrome (Figure 17.14). However, at the end of
exercise, some patients are not able to relax their muscles completely between
contractions because of muscle pain or muscle fatigue, or both. Therefore, muscle
relaxation pressure should always be related to and compared with intramuscular
pressure at rest after exercise (Figure 17.15). If these two pressures are at fairly
similar levels, many pitfalls can be avoided. Examples of such pitfalls are increased
muscle relaxation pressure due to inability to relax muscles or a high muscle contraction frequency.3
MEAN MUSCLE PRESSURE
DURING
EXERCISE
The mean muscle pressure (MMP) is calculated from the muscle contraction pressure
(MCP) and muscle relaxation pressure (MRP) by adding one third of the pulse
pressure to the relaxation pressure according to Equation 17.6:
MMP = MRP + 1/3(MCP MRP)
(17.6)
This means that MMP depends on the MCP and MRP.22 Therefore, MMP is secondary to changes of both these pressures. MMP exceeding 50 to 85 mmHg have
been used as criteria in diagnosing chronic compartment syndrome.46,50 However,
by denition, MMP values depend on both contraction and relaxation pressures.
275
Pressure
A.
B.
C.
Time
FIGURE 17.15 (A) Muscle contraction and relaxation pressures during exercise. At the end
of exercise (B), the subject may have difculties in relaxing their muscles. These patients have
elevated muscle relaxation pressures and elevated intramuscular pressure at rest after the exercise
test. The true muscle relaxation pressure was probably at the same level as the dotted line.
Therefore, the mean pressure is secondary to changes of both these pressures. MMP
is an unreliable and physiologically unrelated parameter to use in diagnosis of
chronic compartment syndrome.3,9,10,65 The level of MMP, measured by methods
with slow dynamic properties, depends also on the relative duration of the contraction
and relaxation. The longer the duration of the muscle contraction is, the higher the
MMP will be (Figure 17.16). Contraction cycles of short duration followed by a
long muscle relaxation time give low mean muscle pressure values. Such recordings
are artifacts from pressure-recording systems with slow dynamic properties that are
due to the contraction frequency and relative duration of the muscle contraction and
relaxation time. Overdamped pressure-recording systems with an increased rise time,
such as the wick catheter system and other noninfusion systems, are prone to cause
this artifact. This is also true for any catheter system that becomes partially occluded.
AT
REST
AFTER
EXERCISE
Normal Values
Intramuscular pressure immediately at rest after exercise is normally between 10 and
25 mmHg, which is fairly equal to the MRP at the end of exercise in a supine subject.
This pressure parameter depends on the volume load of the muscle. Intramuscular
pressure returns to preexercise levels within 5 to 10 min.3,40,46,57,58,60,63,66
Abnormal Values
Pressures exceeding 30 to 35 mmHg at rest after exercise and a time period
exceeding 6 to 10 min to normalize the increased pressure have been used as criteria
to diagnosis the syndrome.2,3,9,16,60 These parameters are useful if MRP during
276
Pressure
A.
B.
Time
C.
FIGURE 17.16 Redrawing from an intramuscular pressure recording during exercise with
(A) an infusion system with good dynamic properties. Pressures during muscle contraction
and muscle relaxation can be recorded. The pressures obtained by a recording system with
slow dynamic properties like some non-infusion uid-lled systems depend on the relative
duration of the contraction. At (B), the contraction and relaxation times are equal. At (C)
(upper trace) the contraction duration is about 80% of the cycle. Therefore, the recorded
pressure increases closer to the true muscle contraction pressure value. At (C) (lower trace)
the contraction duration is about 20% of the cycle. Therefore, the recorded intramuscular
pressure decreases closer to the muscle relaxation pressure.
exercise is not recorded. Increased pressure by active muscle tension due to pain
must be excluded, and external compression by the underlying bed must be avoided.
There is a slight risk of making a false diagnosis of chronic compartment syndrome
if the pressure at rest after exercise is used as the only diagnostic criteria.3 It takes
more than 10 to 20 min to normalize abnormally elevated intramuscular pressure
at rest (Figure 17.14).
Patients with muscular hypertension syndrome have increased intramuscular
pressure at rest after exercise and normal MRP during exercise.3 The reason for this
is their inability to relax their muscles at rest after exercise possibly because of pain
(Figure 17.6). Following the results of pressure monitoring, this condition has been
labeled muscular hypertension syndrome.3 Simultaneous measurements of muscular activity by electromyography (EMG) and intramuscular pressure from the same
spot will help differentiate between the two conditions. In patients with chronic
compartment syndrome, the pressure increase depends only on the volume load of
the compartment. The EMG signal is silent in these patients. On the contrary, patients
with muscular hypertension syndrome have increased intramuscular pressure at rest
after exercise and a positive EMG signal.
INTRAMUSCULAR PRESSURE OSCILLATIONS
AT
REST
AFTER
EXERCISE
Increased amplitude of pulse-synchronous oscillations of intramuscular pressure at

rest after exercise can normally be recorded when the muscle is swollen.3,9,29,37 The
277
pressure amplitude at rest after exercise is signicantly higher in patients with

chronic compartment syndrome (Figure 17.14). This is due to decreased compliance
of the compartment. Pressure amplitude varies with the volume change induced by
each arterial pulse and compliance of the compartment.
ESTIMATION OF FORCE GENERATION AND MUSCLE

LENGTH BY INTRAMUSCULAR PRESSURES
FORCE GENERATION ESTIMATED
BY INTRAMUSCULAR
PRESSURE
AND
EMG
Tensile force is transmitted to the muscle tendon during muscular activity. Stress from
each muscle ber increases intramuscular pressure.20 Figure 17.17 illustrates the pennation angle alpha, which is the angle between the muscle ber and the tendon. It
shows the magnitude and direction of forces generated at the end of each type of
muscular activity. The parallelograms show that the tensile force at the end of eccentric
activation of a muscle ber is transmitted to the tendon at a relatively higher proportion.
The stress that generates the interstitial hydrostatic pressure is lower compared to end
concentric activity when the ber is shorter. The reason for this is the lower pennation
angle at the end of eccentric muscular activity compared with the end of concentric
activity.22 The quota between intramuscular pressure and torque generation during
eccentric muscle contractions is lower than during concentric muscle contractions. The
reason for this is the relatively unchanged intramuscular pressure and increased force
generation during eccentric muscular activity.21,22
An almost spherical muscle with a large ber curvature, i.e., with a short radius,
transmits less force to the tendon than a straight ber does. Most of the tensile forces
are transformed into stresses that are transmitted into muscle tissue as a high interA.
B.
08L
L
2
Ft
Ft
F1
Fs
F2
Fs
FIGURE 17.17 A muscle contraction at the end of eccentric contraction (A) and concentric
contraction (B). The gures are parallelograms illustrating the tensile forces transmitted to
the tendon (Ft) and the compressive forces (Fs), which generate the intramuscular hydrostatic
pressure. Fs is the stress that creates the intramuscular pressure during contraction.
278
5 sec
200 mmHg
IMP
100 mv
EMG
Time
FIGURE 17.18 The close correlation between intramuscular pressure (upper trace) and the
EMG signal (lower trace) from the same muscle during contraction.
stitial hydrostatic pressure. One example of such an extreme muscle is the heart
muscle as a muscle pump. The heart muscle creates intravascular uid hydrostatic
pressures that are high enough to maintain tissue perfusion.
EMG has been used extensively as a technique to monitor force output during
isometric contraction. Some studies report a linear relationship between force and EMG
during isometric contraction,67 whereas other studies report nonlinear.68,69 The use of
EMG as an indicator of contractile force during nonisometric exercise poses additional
problems. EMG is insensitive to changes in ber length and contraction velocity. EMG
represents electrical excitation of muscle rather than its intrinsic mechanical properties
and is therefore reported to be unsuitable for monitoring specic muscle function during
dynamic exercise. Aratow and co-workers showed that intramuscular pressure provides
a more linear index of contraction force than EMG does for the soleus and tibialis
anterior muscles during concentric and eccentric activity.5 Figure 17.18 illustrates the
close relationship between intramuscular pressure and EMG during muscular activity.
FORCE GENERATION
AND
MUSCLE LENGTH
Adjustment of muscle tension is important at tendon transfer and free muscle transfer.
It may be difcult to manually assess the proper tension of the muscle tendon complex
during surgery. Measurement of intramuscular pressure is one possibility to optimize
the tension of a transferred muscle. Another possibility is to measure the sarcomere
length. The goal is to keep the optimal relationship between excursion and sarcomere
length to save the optimal force generation from the bers and thereby joint torque.
SUMMARY
Dynamic properties of a pressure-recording system are important for accurate measurements of intramuscular pressures during exercise. Catheters for pressure recordings
279
should be inserted parallel with muscle bers to minimize physiological reactance.

Bent catheters, partial occlusion, external compression, patient and joint position, as
well as catheter depth in the muscle can result in erroneous pressure recordings. MRP
and intramuscular pressure at rest after exercise are measures on the volume load of
the muscle. They are the most reliable pressure parameters to study in the diagnosis
of chronic compartment syndrome. MCP is a measure of the force generation from
the muscle. MMP during exercise is a physiologically unrelated parameter in the
diagnosis of the syndrome. Neither MCP nor MMP can be used in the diagnosis of
chronic compartment syndrome. Measurements of intramuscular pressure during exercise also include a signicant learning curve. It is an art of electromanometry. A safe
diagnosis of chronic compartment syndrome can be established by combining clinical
examination of the patient following an exercise test that elicits the symptoms with
intramuscular pressure studies.
REFERENCES
1. Allen, M.J. and Barnes, M.R., Exercise pain in the lower leg: chronic compartment
syndrome and medial tibial syndrome, J. Bone Jt. Surg., 68-B, 818, 1986.
tissue pressure measurement in diagnosing chronic anterior compartment syndrome,
Am. J. Sp. Med., 16, 143, 1988.
Am. J. Sp. Med., 16, 165, 1988.
5. Aratow, M., Ballard, R., Crenshaw, A., Styf, J., Watenpaugh, D., Kahan, N. et al.,
Intramuscular pressure and EMG as indices of force during isokinetic exercise, J.
Appl. Physiol., 74, 2634, 1993.
6. Crenshaw, A.G., Karlsson, S., Styf, J., Bcklund, T., and Fridn, J., Knee extension
torque and intramuscular pressure of the vastus lateralis muscle during eccentric and
concentric activities, Eur. J. Appl. Physiol., 70, 13, 1995.
7. Krner, L., Parker, P., Almstrm, C., Andersson, G.B.J., Herberts, P., Kadefors, R. et
al., Relation of intramuscular pressure to the force output and myoelectric signal of
skeletal muscle, J. Orthop. Res., 2, 289, 1984.
8. McDermott, A.G.P., Marble, A.E., Yabsley, R.H., and Phillips, B., Monitoring dynamic
anterior compartment pressures during exercise, Am. J. Sp. Med., 10, 83, 1982.
10. Styf, J., Suurkula, M., and Krner, L., Intramuscular pressure and muscle blood ow
Spine, 12, 680, 1987.
13. Baumann, J.U., Sutherland, D.H., and Hnggi, A., Intramuscular pressure during
walking: an experimental study using the wick catheter technique, Clin. Orthop., 145,
292, 1979.
14. Fridn, J., Sfakianos, P.N., Hargens, A.R., and Akeson, W.H., Residual muscular
swelling after repetitive eccentric contractions, J. Orthop. Res., 6, 493, 1988.
280
16. Veith, R.G., Recurrent compartmental syndromes due to intensive use of muscles,
Compartmental Syndromes, Matsen, F.A. III, Ed., Grune & Stratton, New York, 1980,
p. 133.
17. Styf, J., The venous pump of the human foot, J. Clin. Physiol., 10, 77, 1990.
18. Styf, J., Lundin, O., Petras, S., and Gershuni, D., Prophylactic knee braces impair
local muscle function, Am. J. Sp. Med., 22, 830, 1994.
L., Intramuscular uid pressure during isometric contraction of human skeletal muscle, J. Appl. Physiol., 56, 287, 1984.
Med., 3, 243, 1995.
23. Kirby, R.L. and McDermott, P., Anterior tibial compartment pressures during running
with rearfoot and forefoot landing styles, Arch. Phys. Med. Rehab., 64, 296, 1983.
24. Logan, J.G., Rorabeck, C.H. and Castle, G.S.P., The measurement of dynamic compartment pressure during exercise, Am. J. Sp. Med., 11, 220, 1983.
evaluation of a ber transducer-tipped catheter system, Eur. J. Appl. Physiol., 65,
178, 1992.
28. Shapiro, G.G. and Krovetz, L.J., Damped and undamped frequency responses of
underdamped catheter manometer systems, Am. Heart J., 80, 226, 1970.
30. Fry, D.L., Noble, F.W., and Mallos, A.J., An evaluation of modern pressure recording
systems, Circ. Res., 5, 40, 1957.
31. Stegall, H.F., A simple, inexpensive, sinusoidal pressure generator, J. Appl. Physiol.,
22, 591, 1967.
32. Falsetti, H.L., Mates, R.E., Carroll, R.J., Gupta, R.L., and Bell, A.C., Analysis and
correction of pressure wave distortion in uid-lled catheter systems, Circulation,
49, 165, 1974.
33. Nakhostine, M., Styf, J.R., Leuven, S.V., Hargens, A., and Gershuni, D.H., Intramuscular pressure varies with depth: the tibialis anterior muscle studied in 12 volunteers,
Acta Orthop. Scand., 64, 377, 1993.
34. Styf, J., Crenshaw, A., and Hargens, A., Comparison of non-infusion and non-constant
infusion techniques, Acta Orthop. Scand., 60, 593, 1989.
747, 1989.
281
38. Brace, R.A., Guyton, A.C., and Taylor, A.E., Reevaluation of the needle method for
measuring interstitial uid pressure, Am. J. Physiol., 229, 603, 1975.
by a direct method, J. Clin. Invest., 16, 845, 1937.
wick catheter technique for measurement of intramuscular pressure, J. Bone Jt. Surg.,
58-A, 1016, 1976.
75-A, 231, 1993.
an experimental investigation using the slit catheter, J. Trau., 21, 446, 1981.
J. Orthop. Res., 7, 812, 1989.
45. Barnes, M.R., Gibson, M.J., Scott, J., and Allen, M.J., A technique for the long term
measurement of intra compartmental pressure in the lower leg, J. Biomed. Eng., 7,
35, 1985.
46. McDermott, A.G.P., Marble, A.E., Eng, P., and Yabsley, R.H., Monitoring acute
compartment pressures with the STIC catheter, Clin. Orthop., 190, 192, 1984.
Physiol. Scand., 90, 583, 1974.
48. Guyton, A.C., Interstitial uid pressure: pressure volume curves of interstitial space,
Circ. Res., 16, 452, 1965.
49. Mubarak, S.J., Gould, R.N., Lee, Y.F., Schmidt, D.A., and Hargens, A.R., The medial
tibial stress syndrome: a cause of shin splints, Am. J. Sp. Med., 10, 201, 1982.
patients with chronic comparment syndrome in the leg, J. Bone Jt. Surg., 63-A, 1304,
1981.
51. Crenshaw, A., Styf, J.R., Mubarak, S., and Hargens, A.R., A new beroptic transducertipped catheter for measuring intramuscular pressures, J. Orthop. Res., 8, 464, 1990.
52. Bavetta, S., Norris, J.S., Wyatt, M., Sutcliffe, J.C., and Hanlyn, P.J., Prospective study
of zero drift in beroptic pressure monitors used in clinical practice, J. Neurosurg.,
86, 927, 1997.
53. Sporrong, H., Palmerud, G., Herberts, P., and Styf, J., Comparison of a uid lled
catheter system and a transducer-tipped catheter for intramuscular pressure recordings, submitted, 2003.
14, 1, 1977.
55. Hargens, A.R., Akeson, W.H., Mubarak, S.J., Owen, C.A., Gershuni, D.H., Garn,
S.R. et al., Tissue uid pressures: from basic research tools to clinical applications,
J. Orthop. Res., 7, 902, 1989.
282
56. Nkele, C., Aindow, J., and Grant, L., Study of pressure of the normal anterior tibial
compartment in different age groups using the slit-catheter method, J. Bone Jt. Surg.,
70-A, 98, 1988.
58. Pedowitz, R.A., Hargens, A.R., Mubarak, S.J., and Gershuni, D.H., Modied criteria
for the objective diagnosis of chronic compartment syndrome of the leg, Am. J. Sp.
Med., 18, 35, 1990.
59. Kirkeb, A. and Wisnes, A., Regional tissue uid pressure in rat calf muscle during
sustained contraction or stretch, Acta Physiol. Scand., 114, 551, 1982.
Scand. J. Sci. Sp., 5, 291, 1995.
62. Taheri, S.A., Yacobucci, G.N., Williams, J., and Elias, S., Deep posterior compartment
pressure in the evaluation of venous insufciency of the lower extremity: a preliminary
report, J. Vasc. Dis., 173, 1984.
63. Styf, J. and Krner, L., Chronic anterior compartment syndrome of the lower leg:
65. Rorabeck, C.H., Fowler, P.J., and Nott, L., The results of fasciotomy in the management of chronic exertional comparment syndrome, Am. J. Sp. Med., 16, 224, 1988.
67. Komi, P.V. and Buskirk, E.R., Reproducibility of electromyogrphic measurements
with inserted wire electrodes and surface electrodes, Electromyogr. Clin. Neurophysiol., 10, 357, 1970.
68. Lawrence, J.H. and Luca, C.J.D., Myoelectric signal versus force relationship in
different human muscles, J. Appl. Physiol., 54, 1653, 1983.
69. Solomonow, M.R., Baratta, R., Zhou, B.H., Shoji, H., and DAmbrosia, R., Historical
update and new developments on the EMG-force relationships of skeletal muscles,
Orthopaedics, 9, 1541, 1986.
18
Limb Edema
INTRODUCTION
Edema is defined as an abnormal accumulation of fluid within the interstitial space.

It is a pathological condition and a sign of disturbed microcirculation. The formation
of interstitial edema may alter the tissues nutrition and viability. It may contribute
to tissue hypoxia by increasing the distance that oxygen must diffuse from the
capillary to the cell (Figure 18.1). Another harmful effect of edema is its influence
on the magnitude of fluid transportation over the capillary bed by affecting the
Starling equilibration as discussed in Chapter 1. Edema increases the interstitial fluid
hydrostatic pressure. Therefore, the local perfusion pressure may decrease. Patients
with limb edema may experience discomfort and pain.
EDEMA FORMATION
Edema of a limb is seen by clinical means when the weight of the limb increases
by ca. 10% above normal.1 An exsanguinated human limb will swell by ca. 10% of
its original volume after release of a pneumatic tourniquet.2 This compares to a 5%
increase of limb circumference. The reason for this is the combined effects of reactive
hyperemia and subsequent swelling. During reactive hyperemia, the intravascular
volume further increases. The subsequent swelling is caused by increased interstitial
volume. Following vascular reconstruction, leg volume may increase by up to 26%
on the operated side.3 The interstitial swelling is due to increased microvascular
permeability and the late phase of swelling is due to impaired lymphatic drainage.
In the clinical setting, edema is seen after major orthopedic and vascular surgery
to the extremities, burn injuries, and following fasciotomy due to acute compartment
syndrome. Other reasons for edema formation are different conditions of venous
hypertension. Edema is commonly seen in patients with reperfusion syndromes. Limb
edema can worsen reperfusion injury by increasing vascular resistance and the distance
for oxygen diffusion. Reperfusion of ischemic limbs is associated with a high amputation rate (12 to 22%). Only 60 to 70% of the extremities are functionally intact after
a reperfusion injury.4 Immobilized extremities are also prone to edema formation.
Edema formation can result from disturbances originating in the microvascular
bed, the interstitial space or the lymph vessels. The mechanisms for edema formation
may therefore be classified as vasogenic edema, myxedema, or lymphedema.
VASOGENIC EDEMA
Capillary hypertension, low intravascular oncotic pressure, and alterations of the
microvascular barriers may cause vasogenic edema.
283
284
Capillary 1
Normal diffusion
Capillary 2
Edema diffusion
Capillary 3
FIGURE 18.1 Effect of edema on oxygen diffusion. Edema increases the distance that
oxygen must diffuse through the interstitial space from the capillaries to the cells.
Capillary Hypertension
The most common reason for increased capillary pressure in the trauma situation is
abnormally elevated venous pressure due to obstruction of venous blood flow.
Increased capillary pressure due to arterial hypertension is uncommon. Only 10%
of the arterial pressure increment is transmitted to the capillary level.
Venous stasis induces edema formation5,6 and may even induce acute compartment syndrome in the leg.7,8 Venous hypertension is an important factor for the
development of acute compartment syndrome in the lower limbs.911 Venous return
from the lower limb may decrease by elevated intraabdominal pressure,12,13 by
injuries to the pelvis and proximal thigh14 as well as by extensive thrombosis.15
Gross edema may occur following elevation of venous pressure by 10 to 15 mmHg.
Low Intravascular Oncotic Pressure
Hypoproteinemia is also an uncommon reason for edema in trauma cases. It may
be a contributing factor in patients with cirrhosis who have a low protein synthesis
and in patients with nephrosis who have a rapid escape of plasma proteins.
Alterations of Microvascular Barriers
Tissue injury induces the release of many vasoactive substances, which may alter
vascular tone and endothelial cell function. Edema may be created by increased
capillary filtration following ischemic damage to the endothelial cells.16 In these
conditions, a widening of the interendothelial clefts of the capillary bed occurs. The
pore widening reduces the protein reflection coefficient of the Starling equilibrium.
The osmotic pressure gradient over the capillary, which is the difference between
intravascular osmotic pressure and interstitial osmotic pressure, falls suddenly, and
large volumes of fluid are accumulated in the interstitial space.
Limb Edema
285
Edema following inflammation is caused by a number of vasoactive substances,

which may alter the vascular tone and the endothelial porosity. A 50% increase of
the pore diameter induces a 100% elevation of the interstitial water content.17 The
capillary filtration coefficient may increase fourfold in myocitis.18
MYXEDEMA
In myxedema, the amount of interstitial water and matrix is increased. The condition
may thus be regarded as hypertrophy of the interstitial space. The water and the
interstitial space become organized, which leads to the clinical condition of nonpitting edema. An excess of tyrotropin may induce the condition. Myxedema is also
observed in patients with primary hypothyroidism and hyperthyroidism secondary
to hypersecretion of tyrotropin.17 Patients with Graves disease may have pretibial
myxedema. They have a firm bulging over the anterolateral aspect of the leg proximal
to the lateral malleolus. Patients with a peroneal nerve tunnel syndrome, or entrapment of the superficial peroneal nerve, may also have a similar anterolateral swelling
which is edema of pitting type.19,20
LYMPHEDEMA
Lymphedema may be caused by obstruction of lymph flow.21 It occurs when lymph
flow is reduced to less than 50%.17 Impaired lymph flow may be caused by external
compression that obstructs vascular return from a limb, or by destroyed lymph
vessels, e.g., after dissection during vascular surgery.22,23 Edema of the leg is commonly observed after arterial reconstruction of the lower limbs. Several reasons for
this are possible, as discussed previously. Reduced lymphatic drainage due to intraoperative damage to lymph vessels is an additional possibility.22,23
EDEMA-PREVENTING MECHANISMS
Increased tissue hydrostatic pressure and decreased oncotic pressure in the interstitial
space are two edema-preventing mechanisms.5 The third edema-preventing factor
consists of complex interactions of lymph formation, hydraulic permeability of the
interstitial space, filling hydrostatic pressure of the prelymphatic space, and return
of lymph fluid by the lymphatic vessels. Lymph flow is determined by the magnitude
of capillary filtration. Hydraulic permeability of the interstitial space is a measure
of how easily fluid flows through the interstitial space. Filling pressure in the
prelympathic space is a parameter that depends on interstitial hydrostatic pressure.
Finally, the ability of lymph vessels to transport the lymphatic fluid is important to
prevent lymphedema.24,25
Competent intraluminal valves prevent retrograde lymph flow in most tissues.
However, the lymph vessels in muscle tissue have no contractility and probably lack
valves in the collecting ductuli.26 Lymph flow from skeletal muscle therefore depends
on active and passive muscular action. Contraction of skeletal muscle may empty a
lymph vessel.21 During muscle relaxation or when the extravascular compression is
released, the intraluminar pressure decreases because of a rebound in the walls of
286
the lymph vessels. This creates a suction effect that possibly is transmitted to the
prelymphatic space.
EDEMA-REDUCING METHODS
Limb edema may be reduced by concentric muscular activity, passive stretch of
muscle, external compression of the limb, and limb elevation. Several leg and foot
muscle pumps coordinate to facilitate return of venous blood from the lower limb.
MUSCLE CONTRACTIONS
Muscle contractions work as peripheral venous pumps. Muscular activity lowers
edema by lowering intravenous pressure. Muscular activity also increases lymph
flow.21,27 Intramuscular pressure in the leg is also reduced following muscle contraction of the leg in a standing or sitting subject (Figure 18.2).28 Pressure in different
muscles during contraction increases to 100 to 200 mmHg.2939 The recruitment
pattern and muscle length changes that occur during exercise may provide a more
effective muscle pump than during electrical stimulation.40
PASSIVE STRETCH
OF
MUSCLE
Passive stretch of leg muscles may increase intramuscular pressure fivefold.28,4143

It may also increase lymph flow.21,27,44,45 Intermittent passive muscle stretch oscillates
the interstitial hydrostatic pressure in different leg muscles.28,41,42,46 Pulsations of
hydrostatic pressure in the interstitial space increase lymph flow.26 These pulsations
of hydrostatic pressure may also reduce edema in human legs. Passive muscular
stretch may therefore be a method of treatment in patients with limb edema.
Another clinical application of intermittent passive stretch of muscle is continuous passive motion equipment, which possibly works to reduce edema by limb
elevation and by passive stretch of muscles.
Pressure (mmHg)
40
0
A.
B.
C.
Time
FIGURE 18.2 Pressures in a leg muscle before (A), during (B), and after (C) three active
flexions of the ankle joint in a patient with vein obstruction at the thigh level. Intramuscular
pressure is lower after the contractions due to decreased volume of the leg. Active muscle
contractions are effective in reducing elevated pressure due to venous stasis.
Limb Edema
287
Continuous Compression
External compression of skeletal muscle increases lymph flow.27 Compression stockings are not suitable as an edema-reducing treatment following reconstructive vascular surgery or in patients with imminent acute compartment syndrome. Compression stockings increase interstitial hydrostatic pressure and thereby decrease the local
arteriovenous pressure gradient. The decreased perfusion pressure may lead to
increased risk for limb ischemia in bedridden patients.
Intermittent Compression
Methods for intermittent pneumatic compression of the leg or limb have been used
to treat venous insufficiency, postural edema, and prevent thrombosis.4749 They are
proven to effectively reduce swelling and pain after fasciectomy.50 They may also
be useful in patients following vascular trauma and vascular reconstruction. They
do not mimic the normal action of musculovenous pumps. Intermittent external
compression of the calf muscles is still a controversial method to reduce edema.
The venous plexus of the sole of the human foot operates by weight bearing on
the foot and acts in conjunction with the musclovenous pumps further up the leg.28,51
Neither toe nor ankle movements can empty the venous plexus in the nonweightbearing foot. Passive compression of the sole of the foot by a pneumatic pump gives
oscillations of the interstitial hydrostatic pressure in the leg.28 The mechanism for
this may be intermittent passive muscle stretch of leg muscles (Figure 18.3). The
tendons of leg muscles may be passively stretched by external compression at the
longitudinal arch of the foot (Figure 18.4). Impulse compression of the foot reduces
A.
B.
C.
FIGURE 18.3 Pressure in the flexor digitorum muscle (A) and in the subcutaneous tissue
(B) in a healthy leg without venous stasis. Intramuscular pressure during venous stasis is
shown at (C). The intramuscular pressure oscillations last for about 4 sec, which is the same
time the foot pump is activated. Arrow up indicates the start of pump action and arrow down
indicates the end of activation.
288
The foot at rest
Tendo m. flex. hallucis long.
During
compression
Tendo m. tibialis ant.
External compression
FIGURE 18.4 Foot at rest (A) and during compression by the pneumatic foot pump (B). The
figure illustrates how the tendon to the muscle is deviated when it passes the longitudinal
arch of the foot. The pressure amplitude in the lower leg during pump activation is explained
by passive intermittent muscle stretch. (Redrawn from Styf, J., J. Clin. Physiol., 10, 77, 1990.)
posttraumatic swelling and pain, but cannot reverse abnormally high intramuscular
pressure in patients with acute leg compartment syndrome.52
Treatment by the venous foot pump simulates the effects of weight bearing
by increasing venous return in immobilized patients.28,52 Gardner and Fox51 used
the phlebographic technique to show that mechanical activation of the venous
plexus of the foot could return the venous flow up to groin level without any
assistance of muscular activity. Venous return from the lower extremity may thus
be stimulated by a passive, mechanical activation of the venous plexus of the
foot.28,5153 Venous return by this mechanism is similar to that seen in standing
and walking.
LIMB ELEVATION
The desirable effect of limb elevation early after trauma and surgical treatment
is to diminish local bleeding by decreased perfusion pressure (Figure 18.5). Limb
elevation is recommended as a treatment in patients with venous hypertension
Limb Edema
289
Pressure
MAP
MAP
Perfusion pressure
Perfusion pressure
PV
PV
Normal
IMP
Supine subject
Normal
IM P
Elevated limb
FIGURE 18.5 Normal perfusion pressure in a supine subject with the limb at heart level (left
figure) and the decreased perfusion pressure in an elevated limb. The main effect of limb
elevation is deceased local perfusion pressure due to decreased mean arterial pressure (MAP).
The venous pressure (Pv) remains unchanged.
following trauma.54 However, elevation of a limb that is externally compressed

may impede local muscle blood flow55,56 and may induce dysfunction of the deep
peroneal nerve.56 Limb elevation during prolonged surgery may also induce acute
compartment syndrome.5759 Limb elevation combined with external compression
in patients with arterial disease of the lower limb increases the risks for insufficient perfusion pressure. Finally, limbs should not be elevated in patients with
abnormally elevated intramuscular pressure (or imminent acute compartment
syndrome) because limb elevation may induce ischemia due to decreased perfusion pressure.60 The effects of an elevated limb on the interstitial hydrostatic
pressure, arterial pressure, and the intravenous pressure in healthy individuals
and in patients with abnormally increased tissue pressure are further discussed
in Chapter 4 and Chapter 5.
LEG
AND
FOOT MUSCLE PUMPS
The calf has two ways of acting as a musculovenous pump, one passive, which is
distal, and the other active, which is proximal. The distal muscle pump is activated
by dorsiflexion of the ankle joint. The distal part of the posterior compartments
is narrower than the proximal parts. When calf muscles are pulled distally by ankle
joint dorsiflexion, they are compressed by the osteofascial boundaries of the
posterior compartments. It is believed to function as a conically shaped piston,
which is passively compressed by the osteofascial boundaries of the leg.41,43,52 The
proximal musculovenous pump is activated by concentric muscle contraction
during plantarflexion of the ankle or by eccentric muscle activity during dorsiflexion of the ankle joint.28,52,61
290
Intramuscular pressure in the calf muscles may increase by three ways. First,
pressures may reach 100 to 300 mmHg during concentric and eccentric plantarflexion
of the ankle joint.6264 Second, calf muscles are antagonistically coactivated during
dorsiflexion of the ankle joint to intramuscular pressure values of at least 30 to 60
mmHg. Finally, passive dorsiflexion of the ankle joint may increase pressure in calf
muscles to 40 mmHg.41,43,63
Weight bearing on the foot is a powerful edema-reducing mechanism. It activates
all the leg muscle pumps and empties the venous plexus of the foot.28,51 The muscle
pumps of the leg and foot are synchronized. The most powerful edema-reducing
mechanism is muscle contractions during plantar flexion of the ankle joint. By
intermittent external compression of the foot, the venous maximal flow reaches its
peak when the compression interval is about 1 min.48
TRANSPLANTATION
OF
VENOUS VALVES
Patients with insufficient venous valves in the deep venous system experience swelling, heaviness, and pain in their legs, because of edema. These patients have elevated
intramuscular pressure due to venous insufficiency.15,65 The symptoms may improve
and the muscle relaxation pressure during exercise may normalize by transplantation
of patent venous valves (Figure 18.6). Transplantation of a single valve to the
superficial femoral location of an incompetent venous system may temporarily
correct venous hemodynamics.66 Microsurgical flap reconstruction maintained good
clinical and hemodynamic results over time.67
Pressure (mmHg)
40
Before
0
40
After
0
Time
FIGURE 18.6 Intramuscular pressure recording before and after operation for insufficient
valves. Before surgery (upper trace), MRP is elevated due to the reflux over the valves. After
operation (lower trace), MRP as well as intramuscular pressure at rest after exercise are
normalized as signs of valve competence.
Limb Edema
291
HYPERBARIC OXYGENATION
Treatment by hyperbaric oxygenation increases tissue oxygenation in hypoxic tissues
to levels that maintain viability. It may also reduce edema by vasoconstriction.6870
The increased partial pressure of oxygen in the blood causes vasoconstriction by
direct action on blood vessels.69 The mechanism is supposed to include decreased
blood flow and perfusion pressure to the area of injury. Plasma hyperoxygenation
compensates for the decreased flow associated with vasoconstriction. Improved
tissue oxygenation reduced capillary pressure and decreased edema formation lead
to resorption of extravascular fluid and decreased interstitial fluid pressure.
SUMMARY
Edema is always a sign of disturbed microcirculation. Following trauma or surgery
edema may alter the conditions for tissue nutrition and viability. Patients may
experience swelling, pain, and impaired neuromuscular function. Several active and
passive mechanisms to stimulate peripheral musculovenous pumps are available.
Concentric muscle contraction is probably the most powerful edema-reducing mechanism. Passive muscle stretch and several methods for external compression and
limb elevation are additional methods. Hyperbaric oxygenation improves tissue
oxygenation, reduces capillary pressure, and decreases edema formation.
REFERENCES
1. Guyton, A.C., Interstitial fluid pressure: pressure volume curves of interstitial space,
Circ. Res., 16, 452, 1965.
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2051_IDX.fm Page 295 Thursday, October 2, 2003 10:02 AM
Index
A
Abdominal
acute compartment syndromes (See Acute
abdominal compartment syndrome)
chronic compartment syndromes, 101
Accessory soleus muscle, 204205
Achilles tendinitis, 214
Acute abdominal compartment syndrome, 6,
91101
abdominal wall abnormalities associated with,
97
anuria and, 100
bowel distension and, 93
cardiac effects, 95
cardiovascular collapse, 92
clinical manifestations, 98100
cardiovascular, 99100
renal, 100
respiratory, 99
visceral, 100
defined, 91
edema and, 93
etiology, 9293
hemorrhage and, 93
historical perspectives, 92
incidence, 92
metabolic acidosis and, 99
mortality rate, 91
neurologic effects, 9697
oliguria and, 100
pathogenesis, 9293
pathophysiology, 9397
pulmonary dysfunction and, 92
renal effects, 96
respiratory effects, 94
respiratory failure and, 92
tachycardia, 99
tachypnea and, 99
treatment, 100101
nonsurgical, 100
surgical, 100101
adverse effects, 101
asystole following, 101
severe hypotension and, 101
venous occlusion and, 93
visceral abnormalities associated with, 96
Acute compartment syndrome(s), 5

abdominal, 6, 91101 (See also Acute
abdominal compartment syndrome)
arterial injury and, 11
clinical findings, 47, 61
cystic degeneration and, 136
diagnosis, 4562
direct nerve stimulation in, 60
imaging techniques for, 60
intramuscular pressure measurement in,
5960
pulse oximetry in, 60
stimulation by vibration in, 60
differential diagnosis, 61
etiology, 1724
burn injury and, 23
decreased compartment size and, 2223
exercise-induced and, 19
fascial defect and, 2223
fractures and, 1718
increased compartment volume and,
1720
myalgia and, 23
postoperative hematoma and, 19
prolonged ischemia and, 2022
sickle cell trait and, 23
soft tissue trauma and, 18
viper bites and, 24
viral infections and, 23
foot, 5052
forearm, 5758
gluteal, 5455
hand, 5859
historical perspectives, 913
iatrogenic, 68
incidence, 17
intravascular injections and, 20
leg, 4850
lumbar paraspinal, 55
pathogenesis, 10, 1724
pathophysiology, 10, 3340
peroneal, 49
prolonged ischemia and, 2022
reversible, 11
shoulder, 56
thigh, 5254
295
296
treatment, 10, 1213, 6785

general principles, 6769
untreated, 108, 115
upper arm, 5657
Anesthesia, 194
Aneurysm, 20
Anterior tibial pain, 6, 11, 141
Anticoagulation therapy, 20
Antiinflammatory drugs, 193
Anuria, 100
Arterial blood pressure, 37, 39
Arterial injury, 61, 109
Arterial occlusion, 17, 22
Arterial spasm, 11, 36
Arteriovenous gradient theory, 33
B
Bakers cyst, 14, 212
Biomechanics, 221
convection and, 225
Bunnels method, 123
Burn injury, 23, 100
Bursitis, pes Anserinus, 210
C
Calcaneal fractures, 51
Calf hypertension, 5
Calf muscle cramps, 192
Calf pain, 209
Capillary hypertension, 284
Capillary net fluid flow, 1
Chronic anterior tibial compartment syndrome, 6
Chronic compartment syndrome(s), 56, 141147
abdominal, 101
clinical diagnosis, 161170
dysesthesia and, 161
etiology, 142
exercise and, 143
fascial defects and, 161
foot, 166167, 181182
forearm, 168 182184
hand, 169, 184
historical background, 141142
intramuscular pressure in, 142
leg, 162166, 177181
leg pain and, 189
lumbar spine, 169170, 184
muscle blood flow in, 154
muscular hypertrophy and, 144
muscular oxygenation in, 155156
myositis and, 144

neuromuscular function in, 155
pathogenesis, 10, 142
pathophysiology, 10, 151157
thigh, 167168
trauma and, 143
treatment, 10, 175185
goal of, 175
nonoperative, 176
surgical, 176185
venous hypertension and, 144
Claw toe, 117
Codman transducer-tipped catheters, 246,
271272
Compartment(s), 23
defined, 2
increased volume of contents, 1720
fractures and, 1718
muscle compliance within, 3
Compartment syndrome(s), 36
abdominal, acute, 6 (See also Acute
abdominal syndrome(s))
acute, 5
chronic, 56
defined, 3
Compliance
defined, 3
interstitial space, 230232
recording systems for intramuscular pressure
measurement, 237238, 261
Critical closing pressure, 153154
Crush injury, 51, 52
cardiac arrest and, 134
crush syndrome vs., 131
Crush syndrome, 6, 131137
classification, 135
clinical features, 134135
dermatologic, 134
muscular, 134
neurologic, 135
crush injury vs., 131
etiology, 132133
historical review, 131
laboratory findings, 135
myoglobinuria and, 132
pathogenesis, 133
rhabdomyolysis and, 132
treatment, 135136
nonsurgical, 135136
surgical, 136
Cystic degeneration, 136
Index
297
D
Darcys law, 232
Dermatotraction, 80, 81, 8283
Direct nerve stimulation, 60
Disc herniation, lumbar, 214
Distal intrinsic release, 124
Distal quadricepsplasty, 121
Dorsolumbar compartment, 77
Dysesthesia, 161, 194
E
Edema, 1, 17, 61, 93
exercise-induced, 19
ischemic pain and, 2
limb, 283291
formation, 283285
prevention of, 285286
reduction of, 286291
postoperative reduction, 80
posttraumatic, 2
reduction, 69, 80, 286291
subcutaneous pitting, 46
vasogenic, 283
Elastic tensioning devices, 80
Electrostatic force, 1
Elys test, 119
Epimysiotomy, 75
Escharotomy, 23, 100
Exercise, 141
chronic compartment syndrome and, 143
eccentric, 214
edema and, 19
leg pain and, 189
swelling of muscle tissue during, 151
Exertional compartment syndrome, 6
External compression, 2022
External tissue extender, 80
Extravascular flow system, 223224
F
Fascial defect, 2223, 196
Fasciotomy, 12, 47, 7085
for accessory soleus muscle, 205
complications, 180181, 182
decompression by, 12, 68
dorsolumbar compartment, 77, 184
double-incision, 7374
endoscopic, 179, 180
foot, 71, 72, 181182
forearm, 7879, 182184
gluteal compartment, 75, 76, 77

goals, 70
hand, 79, 184
indications, 70
leg, 7174, 177181
parafibular approach, 71, 73
for peroneal tunnel syndrome, 196
postoperative management, 8084, 184185
edema reduction, 80
hyperbaric oxygenation in, 84
secondary wound closure, 8083
skin grafting in, 84
vacuum-assisted wound closure, 8384
shoulder muscles, 77
success rate, 180, 182
thigh, 75, 76, 182
upper arm, 77
Fiberoptic transducer-tipped catheters, 245,
270271
Fluid reservoir, 224
Foot compartments, 5052, 166167
fasciotomy, 71, 72, 181182
ischemic contracture, 115118
Foot and leg muscle pumps, 289290
Forearm compartments, 5758, 168
fasciotomy, 7879, 182184
Fractures, 17
stress, 189
Free tissue transfer, 126127
G
Gangrene, 109
Gluteal compartments, 5455
fasciotomy, 75, 76, 77
Growing pains, 192
H
Hammertoe, 117
Hand compartments, 5859, 169
fasciotomy, 79, 184
Hematoma, 17
Hemorrhage, 93
Hip arthroplasty, 20
Hohmans sign, 204
Hydrostatic pressure, 1, 227
Hyperbaric oxygenation, 84, 291
Hyperemia, 10
Hypoesthesia, 110, 194
298
Hypotension, limb elevation and, 17

Hypovolemia, 68
Hypoxia, 24
I
Idiopathic compartment syndrome, 6
Influenza infections, 23
Interosseous stripping, 123
Interstitial space, 67, 221233
biomechanics, 225230
compliance, 230232
composition, 221223
function, 223225
elastic support, 224
as extravascular flow system, 223224
as fluid reservoir, 224
force transmission, 225
immunologic, 224
neuromuscular transmission, 225
storage, 224
gel, 221
hydraulic permeability, 230232
pressures, 228230
interstitial, 228229
solid tissue, 229
total tissue, 229230
as scaffold for muscular generation, 224225
Intraabdominal hypertension, 91
Intraabdominal pressure measurement, 9798
direct, 97
indirect, 9798
Intracath catheters, 245
Intramuscular pressure, 12
in chronic compartment syndrome, 142
defined, 1
during exercise, 257279
as measure of force generation, 227
measurement, 12, 5960
catheters for, 238247, 263 (See also
Muscle(s), catheters for pressure
measurement)
compliance of recording system, 237238,
261
distortions in readings from, 265267
estimation of force generation and muscle
length by, 277278
during exercise, 257279
limb position during, 265
medium of signal transmission, 247
physiologic reactance, 242243
quality of, 236237
recording systems, 257263
accuracy, 257
compliance, 237238, 261

distortion of readings from, 265267
dynamic testing of, 262263
maintenance of, 263
natural frequency, 261262
rise time for evaluation of, 259261
at rest, 235252, 272273
at rest, after exercise, 275277
in subatmospheric environment, 251
techniques for, 247251, 267272
infusion, 267269
injection, 248249
noninfusion, 250251, 269
noninvasive, 251252
transducer location for, 245247
volume load of muscle during, 242
noninvasive measurement, 251252
reference values, 272277
Intravascular injections, 20
Intravascular oncotic pressure, 284
Intrinsic pressure, 10
Ischemia, 46
bowel, edema and, 93
pain associated with, 2, 192
prolonged, 2022
arterial occlusion and, 22
external compression and, 2021
limb elevation and, 22
warm, 47
Ischemic contracture(s), 6, 107127
classification, 110111
clinic findings, 110
dystrophic tissue changes in, 112
etiology, 108109
flexor muscle retraction in, 110
of foot muscles, 115118
of forearm muscles, 125126
of gluteal muscles, 121
of hand muscles, 121124
hyperemia and, 10
incidence, 108
laboratory model, 9
of leg muscles, 112115
anterior compartment, 113
lateral compartment, 114
posterior compartment, 114115
mild, 111
moderate, 112
nerve tissue lesions in, 110
pathogenesis, 108109
severe, 112
soft tissue trauma and, 18
surgical management, 112
symptoms, 110
Index
299
of thigh muscles, 118121

of thumb cleft, 124
tissue injury and, 109
treatment, 13, 112, 113, 115, 117118,
119121, 124, 125
decompression in, 113
individualization of, 113
K
Kodiag catheters, 246247, 271272
L
Leg compartments, 6, 113, 148150, 177181
anterior, 113, 162163
fasciotomy, 7174
lateral, 114, 163165
posterior, 114115, 165166
Leg and foot muscle pumps, 289290
Leg muscle(s)
contractures, 112115
cramps, 192
electromyographic evaluation, 214
pain, 189214 (See also Leg pain)
Leg pain, 189214
anterior, 190191
anterolateral, 192199
disc herniation, 214
exercise and, 189
muscle spasms and, 214
overuse injury associated with, 190, 214
posterior, 191, 199212
thrombophlebitis and, 213
varicose veins and, 213
venous claudication and, 213
venous diseases and, 212213
venous insufficiency and, 212213
Limb edema
formation, 283285
prevention, 285286
reducing methods, 286291
external compression, 287288
hyperbaric oxygenation, 291
leg and foot muscle pumps, 289290
limb elevation, 288289
muscle contraction, 286
passive muscle stretch, 286
venous valve transplantation, 290
Limb elevation, 17, 22
hypotension and, 17
Lumbar paraspinal compartments, 55

Lumbar spine, 55, 169170
Lymphedema, 285
M
Mallet toe, 117, 118
March gangrene, 5, 11
Medial tibial syndrome, 200203
clinical examination, 201202
defined, 200
etiology, 200201
signs and symptoms, 201
stress fracture vs., 201, 202
treatment, 202203
Metabolic acidosis, 99
Microvascular barriers, 284285
Microvascular occlusion, 152153
Muscle(s)
accessory soleus, 204205
biomechanics, 221
blood flow, 33, 37
arteriovenous gradient theory, 3335
autoregulatory compensation for
decreased, 37
in chronic compartment syndrome, 154
critical closing pressure theory, 35
microvascular occlusion theory, 35
regulation of, 152154
tidal wave theory, 3536
catheters for pressure measurement, 238247
classification of, 243251
Codman transducer-tipped, 246, 271272
contact area, 242
fiberoptic transducer-tipped, 245,
270271
insertion-related tissue trauma, 239, 241
insertion technique for, 238, 263264
intracath, 245
Kodiag, 246247, 271272
myopress, 244245
needle designs, 243244
occlusion of, 241242
position of, 265
response and location of tip, 239
slit, 244
solid-state intracompartmental, 245, 271
tip design, 243
transducer-tipped, 245, 246, 269270
wick, 244
wick-in-needle, 245
compliance, 3
contraction pressure, 227
cramps, 192
300
extracellular matrix, 223

hypertension syndrome, 199
hypertrophy, 144
lipoma, 214
oxygenation, 3738
pain, 191192
inflammatory, 192
ischemic, 192
mechanical, 192
passive stretch of, 286
relaxation during exercise, 273274
skeletal, 191192
spasms, 214
strain, 192, 203204
tissue swelling during exercise, 151
transplantation, 126
volume load, 242
Muscle belly syndrome, 214
Muscle relaxation pressure, 146, 154, 173, 266,
267, 270, 273, 274
Muscular hypertension syndrome, 199, 205207
Myalgia, 23
Myoglobinuria, 132
Myopress catheters, 244245
Myositis, 144, 192
Myxedema, 285
N
Nerve conduction velocity, 38
Nerve entrapment, 189, 191
peroneal, 194
saphenous, 210211
suralis, 211212
tibialis, 209210
Nerve stimulation, direct, 60
Neurapraxia, 61
Neuromuscular function, 38
O
Oliguria, 100
Osmotic pressure, 1
Overload injuries, 144145
Overuse injuries, 190, 214
Oxygenation, muscular, 3738
P
Pain, 61, 110
anterior tibial, 6, 11
exercise-related, 141, 189
growing, 192
ischemia and, 2
leg, 189214 (See also Leg, pain)
Paresis, 61, 110
Paresthesia, 61, 110
Perfusion pressure, 3335, 152
Periostalgia, 192
Periostitis, 192
Peroneal compartments, 49
Peroneal nerve entrapment, 194
Peroneal tunnel syndrome, 194196, 214
pes Anserinus bursitis, 210
Physiotherapy, 193
Pneumatic antishock garments, 93
Polyneuropathy, 194
Popliteal artery entrapment, 207209
tibialis nerve entrapment and, 209
Postthrombotic syndrome, 143
Proximal syndesmosis, 199
Pulse oximetry, 60
R
Range of motion, 46, 61
Recurrent compartmental syndrome, 6
Reperfusion, postischemic, 69
Reperfusion syndrome, 11
Restless leg, 192
Rhabdomyolysis, 5, 23, 131, 132
pain and, 192
S
Saphenous nerve entrapment, 210211
Scintigraphy, 199, 202
Shear stresses, 227
Shoulder compartments, 56
fasciotomy, 77
Sickle cell trait, 23
Skin grafting, 84
Slit catheters, 244
Smith-Pedersen approach, 119
Soft tissue trauma, 18
Soleus muscle, accessory, 204205
Solid-state intracompartmental catheters, 245,
271
Spasm, arterial injury and, 11
Spinal stenosis, 189
Starling equation, 1
Starling-Landis equation, 229
Starling valve theory, 36
Staverman reflection coefficient, 229
Stimulation by vibration, 60
Stress fracture(s), 189
Index
301
fibular, 198199
medial tibial syndrome vs., 201, 202
tibial, 197198, 206207
Suralis nerve entrapment, 211212
Surgical decompression, 12
Syndesmosis, proximal, 199
T
Tachycardia, 99
Tachypnea, 99
Tendinitis, 192
Achilles, 214
medial tibial syndrome and, 200
Tendinosis, 199
Tenodesis effect, 110
Thigh compartments, 5254, 167168
fasciotomy, 75, 76, 182
Thrombophlebitis, 213
Thumb cleft, 124
Tibialis nerve entrapment, 209210
popliteal artery entrapment and, 209
Tidal wave theory, 154
Tinels sign, 194, 209, 212
Traction periostitis, 192
Transducer-tipped catheters, 245, 246, 269270
V
V-Y lengthening, 120
Varicose veins, 213
Vasogenic edema, 283
Venous claudication, 213
Venous hypertension, 1011, 37
neuromuscular function and, 11
Venous occlusion, 61, 93, 108
Venous thrombosis, effort-induced, 213
Venous valve transplantation, 290
Viral infections, 23
Volkmanns contracture, 107
W
Wick catheters, 244
Wick-in-needle catheters, 245
Wire sutures, 80
Wolfs law, 225
Z
Z-lengthening, 120
U
Upper arm compartments, 5657
fasciotomy, 77
2051_color_insert
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COLOR FIGURE 6.6 Intraoperative photo of the lateral thigh. The skin incision should be
complete from the greater trochanter to the lateral femoral condyle.
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(A)
(B)
(C)
COLOR FIGURE 6.12 Secondary wound closure by wire sutures in a patient 3
days after fasciotomy for acute compartment syndrome of the thigh. (A) The lateral thigh wound 3 days after fasciotomy. (B) Wire sutures are applied 3 days after fasciotomy. (C) On Day 5 the sutures are tightened to completely close the wound.
2051_color_insert
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COLOR FIGURE 8.3 Ischemic contracture following untreated acute compartment syndrome of the left leg. The
left side shows a short cavus foot with
an equinu-varus deformity. The distance between the lateral malleolus and
the Achilles tendon (black bar) is shorter.
COLOR FIGURE 8.4 Mild claw toe deformities of dig. II to IV

in patient with ischemic contracture of the flexor digitorum longus muscle and intrinsic dysfunction. The soft tissues along the longitudinal arch
are hypotrophic. The foot is shorter and has a cavus deformity.
2051_color_insert
10/23/03
3:38 PM
Page 4
(A)
(B)
(C)
(D)
COLOR FIGURE 16.3 Pictures of catheter insertion. (A) After the muscle fascia has been
penetrated the steel needle should be withdrawn a few millimeters into the plastic sheath of
the introducer. (B) In this way the cutting tip of the needle will not traumatize the muscle
tissue when the introducer is advanced parallel with the muscle fibers into the preferred
position. (C) The steel needle is retracted and (D) replaced by the pressure-recording
catheter. Finally, the plastic sheath of the introducer is removed.

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COMPARTMENT

2051_C00.fm Page 2 Tuesday, October 14, 2003 11:28 AM

Jorma Styf, M.D., Ph.D.

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Library of Congress Cataloging-in-Publication Data

Visit the CRC Press Web site at www.crcpress.com

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2051_C00.fm Page 10 Tuesday, October 14, 2003 11:28 AM

2051_bookTOC.fm Page 1 Monday, October 6, 2003 2:15 PM

Denitions and Terminology ...............................................................1

Historical Perspectives of Acute Compartment Syndrome .................9

Etiology and Pathogenesis of Acute Compartment Syndrome .........17

2051_bookTOC.fm Page 2 Monday, October 6, 2003 2:15 PM

Decreased Size of the Compartment .............................................................22

Pathophysiology of Acute Compartment Syndrome .........................33

Diagnosis of Acute Compartment Syndrome....................................45

2051_bookTOC.fm Page 3 Monday, October 6, 2003 2:15 PM

2051_bookTOC.fm Page 4 Monday, October 6, 2003 2:15 PM

Treatment of Acute Compartment Syndromes ..................................67

Acute Abdominal Compartment Syndrome ......................................91

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2051_bookTOC.fm Page 6 Monday, October 6, 2003 2:15 PM

Clinical Findings ................................................................................110

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Distal Intrinsic Release.............................................................124

The Crush Syndrome .......................................................................131

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Chapter 10 Etiology and Pathogenesis of Chronic Compartment Syndrome ...141

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Chronic Compartment Syndrome in the Thigh ...........................................167

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Skeletal Muscle Pain ..........................................................................191

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Stress Fractures of the Posteromedial Margin of the Tibia...............206

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Regeneration of Muscle Tissue ..........................................................224

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Force Generation Estimated by Intramuscular Pressure and EMG.....277

2051_C01.fm Page 1 Thursday, October 2, 2003 9:26 AM

Intramuscular pressure is defined as the fluid hydrostatic pressure in the interstitial

2051_C01.fm Page 2 Thursday, October 2, 2003 9:26 AM

Compartment Syndromes: Diagnosis, Treatment, and Complications

sure is regarded to be a scalar-like fluid hydrostatic pressure. It has a magnitude

COMPARTMENT AND COMPLIANCE

2051_C01.fm Page 3 Thursday, October 2, 2003 9:26 AM

Definitions and Terminology

The contents of a compartment are sometimes surrounded by relatively unyielding

2051_C01.fm Page 4 Thursday, October 2, 2003 9:26 AM

Compartment Syndromes: Diagnosis, Treatment, and Complications

2051_C01.fm Page 5 Thursday, October 2, 2003 9:26 AM

Definitions and Terminology

ACUTE COMPARTMENT SYNDROME

CHRONIC COMPARTMENT SYNDROMES

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Compartment Syndromes: Diagnosis, Treatment, and Complications

OTHER CONDITIONS OF ABNORMALLY ELEVATED

THE INTERSTITIAL SPACE

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Definitions and Terminology